Negotiating trust on health-related online forums

Posted on 06/29/2016 by wames

Research abstract:

The internet is increasingly being used as a source of health advice and information by individuals with long term conditions (LTCs). Specifically, online forums allow people to interact with others with similar conditions. However, it is not clear how online health information is assessed by those with LTCs.

This study aims to address this gap by exploring how individuals with contested and uncontested LTCs utilise internet forums. Semi-structured interviews were conducted with 20 participants with ME/CFS and 21 participants with type 1 and 2 diabetes and analysed using thematic analysis.

Participants were recruited via online and offline routes, namely forums, email lists, newsletters, and face-to-face support groups. The findings indicate that the use of online forums was a complex and nuanced process and was influenced by a number of individual and illness-specific factors.

Participants trusted those with similar experiences and perspectives as themselves, while also valuing conventional biomedical information and advice. By accessing support online, forum users were able to draw on a personalised form of support based on the lived experiences of their peers. However, the role of digital literacy in developing and maintaining online relationships must be acknowledged.

‘You get to know the people and whether they’re talking sense or not’: Negotiating trust on health-related forums, by Ellen Brady, Julia Segar, Caroline Sanders in Social Science & Medicine, vol 162, Aug 2016, pp 151–157 [published online 18 June 2016]

Posted in News | Tagged , , , , | Comments Off on Negotiating trust on health-related online forums

The ‘all in the mind’ myth of ME/CFS

Posted on 06/29/2016 by wames

Nursing in practice article, by Dr Keith Geraghty, 27 June 2016: The ‘all in the mind’ myth of myalgic encephalomyelitis/chronic fatigue syndrome

Health professionals should be made aware that ME/CFS is not a psychological illness and in order to improve patient care, nurses need to better understand this illness and its impact on patients.

Nurses often witness close-up the impact of acute and chronic illness on patients. Myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS) is one illness that nurses may encounter that causes profound life changes for many sufferers. This controversial illness is sometimes presented as a psychosomatic disorder that requires psychological treatment. However, there is no compelling evidence that ME/CFS is a mental health condition and increasing evidence shows it is a biological disease with a range of complex symptoms. This article discusses how the ‘all in the mind’ myth of ME/CFS has permeated both medical discourse and popular culture, with negative consequences for patients living with this poorly understood condition.

1. Is ME/CFS really a mental illness?

In a recent Nursing in Practice article, Roberts (2016)1 suggests that ME/CFS is a psychosomatic disorder, best treated with psychotherapy and mindfulness. The erroneous idea that mindfulness is an optimum treatment masks a hidden and more important story; that very little is understood about ME/CFS and many health professionals are sceptical about whether ME/CFS is even a real illness. For example, NICE guidelines do not mention mindfulness.2

A GP once exclaimed to me that ‘all these patients need is anti-depressants and a good pair of running shoes’. While discussing my ME/CFS research at a hospital in Leicester a nurse offered me a similar opinion by suggesting that ‘ME/CFS patients would get out of bed if you paid them £5000 per day’. Such negative views among doctors and nurses are not uncommon and are perhaps fueled by misinformation about the illness being psychological.

In a recent book, All in Your Head: True Stories of Imaginary Illness,3 Dr Suzanne O’Sullivan, a London-based consultant neurologist, includes a chapter on ME/CFS. O’Sullivan argues ME/CFS is strongly associated with psychological complaints and illness beliefs. In contrast, a growing body of scientific evidence suggests that ME/CFS is not an imagined illness, nor is it a psychological condition, but a complex biological disease that is often triggered by an infection that causes observable neuro-immune dysfunction. Far from being ‘all in the mind’, sufferers often experience life-changing and disabling physical symptoms and physiological abnormalities (see Table 1).

Table 1: Biological abnormalities observed in ME/CFS

  • Alterations in grey and white brain matter.
  • Muscle cell dysfunction
  • Immune cell abnormalities
  • Raised inflammatory markers
  • Cellular and oxidative stress
  • Autonomic irregularities.
  • Cardiovascular deficiencies.
  • Orthostatic intolerance.

The World Health Organization (WHO) classifies ME as a neurological disorder in the International Classification of Diseases (ICD-10: G 93.3; WHO, 1992).4

The US Institute of Medicine (2015) conducted an extensive review of the evidence and concluded that ME/CFS is ‘a serious, chronic, complex, systemic disease’.5

The US National Institutes for Health confirmed ME/CFS as a disabling physical illness and stated that the medical profession has been responsible for causing distress to patients with ME/CFS by ignoring patients’ calls for medical help and failing to adequately research the disease.6

2. So why is ME/CFS treated with psychotherapy?

Psychiatrists have long been interested in attempting to explain the medically unexplained. Sigmund Freud, the father of modern psychiatry, explored the connection between the mind and health. The famous French neurologist J. Charcot believed traumatic life events may bring about a form of hysteria or paralysis in patients; while George Beard put forward the theory of neurasthenia (exhaustion of energy within the nervous system).7  These theories continue to influence how doctors perceive medically unexplained illnesses, particularly ME/CFS.

A brief time-line of how ME (nuero-immune disease) became CFS (a psychosomatic fatigue syndrome)

1955: Melvin Ramsay describes a viral outbreak illness among staff at the Royal Free Hospital in London as a post-infectious disease affecting brain, nerves and muscle tissue (Myalgic Encephalomyelitis).

1970s: UK psychiatrists McEvedy and Beard state that ME is nothing more than a case of ‘mass hysteria’.

1980s: A London newspaper runs a story about ME being ‘Yuppie Flu’. Since then, ME has been indelibly linked with stressed-out professionals complaining about exhaustion.

1988: The US Centers for Disease Control recommend replacing ME with a new syndrome (Chronic Fatigue Syndrome).

1990s: UK psychiatrist Simon Wessely argues ME (now CFS) is a biopsychosocial syndrome, partly created by social trends and maintained by patients’ illness beliefs and behaviours.

2000s: Colleagues of Wessely, including nurse/researcher Professor Trudie Chalder, conduct clinical trials of psychotherapy to treat CFS, including the £5 million PACE trial testing cognitive behavioural therapy and graded exercise therapy.8

2007: The UK National Institute for Health and Care Excellence (NICE) conducts a review and recommends CBT and GET for the treatment of ME/CFS.2  This decision is criticised by ME/CFS patient groups who deem CBT and GET inappropriate treatments. In particular, GET attracts much criticism.

2015: A large patient survey finds CBT has little impact on the condition: 74% of patients report that GET makes their symptoms worse, while simple pacing is preferred by patients.9  Such concerns are echoed in scientific studies that suggest exercise therapy may be harmful, given biological abnormalities found in ME/CFS.10

3. So, does cognitive therapy or exercise therapy help anyone with ME/CFS?

The answer to this question is rather complex. ME/CFS is an umbrella term often used for patients with ongoing unexplained fatigue. Hooper (2006) points out that ‘Amorphous definitions and diagnostic symptom criteria have contaminated study cohorts and corrupted research data’.11  Essentially, it may be difficult to differentiate patients with ME/CFS from patients with fatigue or depression, given the generality of the diagnostic criteria for CFS: patients are often lumped together in studies, with depressed patients responding better to CBT compared with ME/CFS patients.12

In addition, CBT may help with the secondary depression or anxiety that occurs in most illness states. Clinical trials of CBT and GET tend to recruit mild to moderately unwell CFS patients, as more severe cases are too unwell to take part. Yet, even if we accept these research biases, the evidence for the success of psychological or exercise therapies in ME/CFS is unconvincing:

  • Cochrane review:A meta-analysis found that while CBT and/or GET may benefit some patients with ME/CFS in the short term, the benefits are short-lived and have little impact on restoring physical function over the long term.13
  • PACE trial:The largest clinical trial of CBT and GET for CFS reported that 22% of patients recovered following CBT/GET added to standard care, while only 7% did after standard care alone.14 However, ‘recovery’ here did not mean a return to normal physical function. A patient could be deemed recovered with a SF-36 (quality of life) score of 60/100 or higher,8 even though a score of 65/100 indicates severe disability with 57/100 being a score of patients with Class II congestive heart failure.15 At follow-up, two years after treatment, there was no clear benefit of adding CBT or GET to standard medical care.8
  • FINE trial: A study of nurse-provided community-based CBT and GET for 296 CFS patients failed to find any evidence for the long-term effectiveness of these therapies.16  FINE stood for ‘Fatigue Intervention by Nurses Evaluation’. CBT-GET was compared against a supportive listening treatment. The FINE investigators found no statistically significant benefits to either pragmatic rehabilitation (CBT-GET) or supportive listening at 70 weeks. The authors concluded that the community setting was inappropriate, rather than the psychotherapy treatment.

4. Why is it important to know the facts?

In a recent Centers for Disease Control ‘Grand Rounds’ event (2016) discussing ME/CFS research, Professor Anthony Komaroff of Harvard University stated that the medical profession were wrong to adopt the name Chronic Fatigue Syndrome in 1988, as this term led to inaccurate perceptions of the illness. Komaroff points out that that there are thousands of published articles on biological dysfunction in ME/CFS, with no compelling evidence to suggest the illness is psychogenic (an illness of the mind).16

Many ME/CFS sufferers and advocacy groups are deeply concerned about the portrayal of the disorder as a psychological illness in medical publications and the wider media. Misinformation may negatively impact patients. Patient surveys consistently reveal that many ME/CFS patients experience medical scepticism, difficult interactions with health professionals and poor care quality (AfME, 2001).17  Sufferers report finding it difficult accessing benefits and social care and often have to fend off accusations of laziness and hypochondria – perhaps a consequence of the perception that the illness is a self-generated psychological illness.

The 25% ME Group, a charity that supports the most severely ill sufferers, state that the medical establishment has largely ignored these ME/CFS patients.18 Many are housebound or bedbound, with family members as full-time care-givers.

We must consider the harrowing case of Miss Sophia Mirza, a young ME sufferer forcibly removed from her home and sectioned under the Mental Health Act to impose psychiatric treatment on her. Miss Mirza died in 2005 and is one of the first patients in the UK to have ME as the official cause of death. The reality that ME/CFS kills some patients and dramatically shortens life expectancy is rarely reported in the media. In addition, ME/CFS sufferers are six times more likely to commit suicide compared to the general population;19 most likely as the result of having to deal with debilitating symptoms, such as chronic pain and sleep deprivation, but perhaps also having to deal with feelings of social isolation and poor medical treatment.

5. What can nurses do to support ME/CFS patients?

Many nurses will encounter ME/CFS patients, particularly in primary care. Nurses often have the capacity to form close therapeutic relationships with patients. Offering empathy and understanding to patients experiencing distressing symptoms is a central part of the nursing role. In the absence of a cure for ME/CFS, nurses are well placed to provide supportive care. By understanding the symptoms generated by the illness, nurses may be able to offer patients better care. ME/CFS severity varies from mild to severe and patients experience the illness in different ways. Some sufferers may be able to continue work on a limited basis, while others may be bed-bound, reliant on family and carers. Retired nurse Greg Crowhurst, a care-giver to a wife with severe ME/CFS, writes eloquently about how nurses may support patients with the illness.19

Practical tips for nursing practice are as follows:

  • Sufferers experience profound fatigue – nurses may be able to ensure patients are not left in waiting areas for long periods of time.
  • Sufferers experience cognitive problems – nurses may assist patients in medical consultations, perhaps asking whether the patient understands the information provided.
  • Sufferers experience sensory overload – nurses may ask patients if they require a quiet area or darkened room, or on home visits, nurses may avoid causing sensory distress by speaking quietly and ensuring mobile phones are turned off.
  • Sufferers symptoms vary and fluctuate – nurses should liaise with family members or care-givers to get a personalised account of the patient’s health status and care needs.
  • Sufferers often feel disbelieved and anxious – nurses may reassure patients, particularly if they convey empathy and knowledge of the illness to the patient.

Nurses also have an another important role as advocates for ME/CFS patients, helping to liaise between the patient and doctor and also helping to promote the patient voice in the public domain. However, to fulfill this important role, nurses need to better understand the illness and to understand that ME/CFS is by no means ‘all-in-the-mind’.

Conclusion: The key message for nurses

Most people feel fatigued following illness, stressful events, or after working long hours. This is quite different from the severe fatigue and the range of symptoms that patients with ME/CFS endure, including: unrelenting painful joints and muscles; cognitive dysfunction, including memory problems; gastrointestinal complaints; transient paralysis; hypersensitivity to light, noise and touch; unrefreshing sleep; post-exertional malaise after minimal effort; and the inability to maintain an upright posture for any significant period.

Overwhelming evidence shows that these symptoms are not psychosomatic. Nurses have a valuable role to play in assisting and supporting patients with ME/CFS. Nurses should not underestimate the power and importance of the nursing position to relieve suffering, prevent harm and promote better care for ME/CFS patients.

References

1. Roberts D. Diagnosing and managing chronic fatigue syndrome. Nursing in Practice 2016, 89.

2. NICE. Chronic fatigue syndrome/myalgic encephalomyelitis (or encephalopathy) – Diagnosis and management of CFS/ME in adults and children. NICE 2007, 53. https://www.nice.org.uk/guidance/cg53/chapter/1-guidance

3. O’Sullivan S. All in Your Head: True Stories of Imaginary Illness, 2016.

4. WHO. International Classification of Diseases, Tenth Revision (ICD-10). WHO 1992; G93.3.

5. IOM (Institute of Medicine). Beyond myalgic encephalomyelitis/chronic fatigue syndrome: redefining an illness. Washington, DC; 2015. ISBN: 978-0-309-31689-7.

6. Green CR, Cowan P, Elk R, O’Neil KM, Rasmussen AL. National Institutes of Health pathways to prevention workshop: Advancing the research on Myalgic Encephalomyelitis/chronic fatigue syndrome. Annals of Internal Medicine 2015;16;162(12):860-865.

7. Beard G. Neurasthenia, or nervous exhaustion. The Boston Medical and Surgical Journal 1869;217-221.

8. White PD, Goldsmith KA, Johnson AL et al. Recovery from chronic fatigue syndrome after treatments given in the PACE trial. Psychological Medicine 2013;43(10):2227-2235.

9. ME Association. ‘ME/CFS Illness Management Survey Results: No decisions about me without me’. Patient Survey, May 2015. http://www.meassociation.org.uk/wp-content/uploads/2015-ME-Association-Illness-Management-Report-No-decisions-about-me-without-me-30.05.15.pdf

10. Twisk F, Geraghty K. Deviant Cellular and Physiological Responses to Exercise in Myalgic Encephalomyelitis and Chronic Fatigue Syndrome. Jacobs Journal of Physiology 2015;1(2):007, 2015.

11. Hooper M. Gibson Inquiry – Day 1 April 18th 2006 – Group Testimonies, Comments by Professor Malcolm Hooper 21st April, 2006. http://www.meactionuk.org.uk/Hooper_on_Gibson_Inquiry_Day_One.htm

12. Jason LA, Torres-Harding S, Brown M et al. Predictors of change following participation in non-pharmacologic interventions for CFS. Tropical Medicine and Health 2008;36(1):23-32. DOI: 10.2149/tmh.36.23.

13. Price JR, Mitchel E, Tidy E, Hunot V. Cognitive behaviour therapy for chronic fatigue syndrome in adults. Cochrane Database of Systematic Reviews 2008, Issue 3.

14. Sharpe M, Goldsmith KA, Johnson AL, Chalder T, Walker J, White PD. Rehabilitative treatments for chronic fatigue syndrome: long-term follow-up from the PACE trial. The Lancet Psychiatry 2015a;2(12):1067-1074.

15. Juenger J, Schellberg D, Kraemer S, Haunstetter A, Zugck C, Herzog W, Haass M. Health related quality of life in patients with congestive heart failure: comparison with other chronic diseases and relation to functional variables. Heart 2002;87(3):235-241. http://dx.doi.org/10.1136/heart.87.3.235

16. Wearden A, Dowrick C, Chew-Graham C et al. Nurse led, home based self help treatment for patients in primary care with chronic fatigue syndrome: randomised controlled trial. British Medical Journal 2010;340:c1777.

16. Komaroff AL. Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A Real Illness. Annals of Internal Medicine 2015;162:871-872.

17. Action for ME. ‘Severely neglected’. Patient Survey, 2001.

18. 25% ME Group. Stakeholder Response to NICE CG53 Three Yearly Review, Nov, 2010. http://www.angliameaction.org.uk/docs/25megroup-nice-cg53-response-nov2010.pdf (accessed January 2016).

19. Roberts E, Wessely S, Chalder T et al. Mortality of people with chronic fatigue syndrome: a retrospective cohort study in England and Wales from the South London and Maudsley NHS Foundation Trust Biomedical Research Centre (SLaM BRC) Clinical Record Interactive Search (CRIS) Register, Lancet, (published online Feb 9.), 2016.

20. Crowhurst G. Supporting people with severe myalgic encephalomyelitis. Nursing Standard 2005;19(21):38-43.

About the Author
Dr Keith Geraghty
Honorary Research Fellow, Centre for Primary Care, University of Manchester

Posted in News | Tagged , | Comments Off on The ‘all in the mind’ myth of ME/CFS

The difficulties of studying whether negative illness beliefs contribute to maintenance of CFS symptoms

Posted on 06/28/2016 by wames

Review abstract:

PURPOSE:

Chronic fatigue syndrome (CFS) is characterized by severe and debilitating fatigue. Studies based on self-report measures suggest negative illness representations, related symptom interpretations, and heightened symptom focusing are maintaining factors of fatigue. This study reviews studies which have investigated these cognitive biases using experimental methods, to (1) review the evidence for information processing biases in CFS; (2) determine the nature of these biases, that is the stages cognitive biases occur and for what type of stimuli; and (3) provide directions for future methodologies in this area.

METHODS:

Studies were included that measured attention and interpretation bias towards negative and illness-related information in people with CFS and in a comparison group of healthy controls. PubMed, Ovid, CINAHL, PsycINFO, Web of Science, and EThOS were searched until December 2014.

RESULTS:

The evidence for cognitive biases was dependent on the methodology employed as well as the type and duration of the stimuli presented.

Modified Stroop studies found weak evidence of an attentional bias in CFS populations, whereas visual-probe studies consistently found an attentional bias in CFS groups for health-threatening information presented for 500 ms or longer. Interpretative bias studies which required elaborative processing, as opposed to a spontaneous response, found an illness-related interpretive bias in the CFS group compared to controls.

CONCLUSIONS:

Some people with CFS have biases in the way they attend to and interpret somatic information. Such cognitive processing biases may maintain illness beliefs and symptoms in people with CFS.

This review highlights methodological issues in experimental design and makes recommendations to aid future research to forge a consistent approach in cognitive processing research.

Statement of contribution

What is already known on this subject? Studies based on self-report measures suggest negative illness representations, related symptom interpretations, and heightened symptom focusing contribute to the maintenance of chronic fatigue. Experimental studies in other clinical populations, such as patients with anxiety, depression, and chronic pain, have identified illness-specific biases in how information is implicitly attended to and interpreted, which has a causal role in these conditions.

What does this study add?

This is the first review of implicit cognitive processes in chronic fatigue syndrome (CFS).
Sustained attention and negative interpretations of somatic information may reinforce negative illness beliefs. Cognitive processes have a role to play in the cognitive behavioural model of CFS.

Attentional and interpretive bias towards illness-related information in chronic fatigue syndrome: A systematic review, by A Hughes, C Hirsch, T Chalder, R Moss-Morris in Br J Health Psychol. 22 June 2016 [Epub ahead of print]

Posted in News | Tagged , , , , , | Comments Off on The difficulties of studying whether negative illness beliefs contribute to maintenance of CFS symptoms

Activity pacing is associated with better & worse symptoms in long term conditions

Posted on 06/28/2016 by wames

Research abstract:

Background:
Activity pacing has been associated with both improved and worsened symptoms, and its role in reducing disability among patients with long-term conditions has been questioned. However, existing studies have measured pacing according to uni-dimensional subscales, and therefore the empirical evidence for pacing as a multifaceted construct remains unclear. We have developed a 26-item Activity Pacing Questionnaire (APQ-26) for chronic pain/fatigue containing five themes of pacing: activity adjustment, activity consistency, activity progression, activity planning and activity acceptance.

Objective:
To assess the associations between the five APQ-26 pacing themes and symptoms of pain, physical fatigue, depression, avoidance and physical function.

Methods:
Cross-sectional questionnaire design study. Data analysed using multiple regression.

Participants:
257 adult patients with diagnoses of chronic low back pain, chronic widespread pain, fibromyalgia and chronic fatigue syndrome/myalgic encephalomyelitis.

Results:
Hierarchical multiple regression showed that activity adjustment was significantly associated with increased physical fatigue, depression and avoidance, but decreased physical function (all P<=0.030). Activity consistency was associated with decreased pain, physical fatigue, depression and avoidance but increased physical function (all P<=0.003).
Activity planning was associated with reduced physical fatigue (P=0.025) and activity acceptance was associated with increased avoidance (P=0.036).

Conclusion:
Some APQ-26 pacing themes were associated with worse symptoms and others with symptom improvement. Specifically, pacing themes involving adjusting/reducing activities were associated with worse symptoms, whereas pacing themes involving undertaking consistent activities were associated with improved symptoms. Future study will explore the causality of these associations to add clarification regarding the effects of pacing on patients’ symptoms.

Activity pacing is associated with better and worse symptoms for patients with long-term conditions, by Deborah Antcliff, Malcolm Campbell, Steve Woby, Philip Keeley in The Clinical Journal of Pain, 17 June 2016 [Preprint]

Posted in News | Tagged , | Comments Off on Activity pacing is associated with better & worse symptoms in long term conditions

Gastric enterovirus infection: a possible cause of gastroparesis

Posted on 06/27/2016 by wames

Research abstract:

BACKGROUND: Gastroparesis (GP) is a disabling chronic gastroenterologic disorder with high morbidity that severely impacts patients’ quality of life. GP can present acutely after a viral-like gastrointestinal illness resulting in speculation that in some patients, neurologic damage caused by the infection might underlie the pathogenesis of idiopathic gastroparesis (IGP).

AIMS: The aim of this study is to document case reports of Enterovirus (EV) infection as a possible cause of IGP.

METHODS: Eleven patients referred with a diagnosis of GP underwent workup to exclude known causes of GP. Those with a history of flu-like symptoms or gastroenteritis prior to onset of GP symptoms had gastric biopsies taken during upper endoscopy to assess for the presence of gastric mucosal EV infection. Data on presenting symptoms, extra-intestinal symptoms and conditions, prior nutritional support requirements, upper endoscopy findings, and response to therapy were cataloged.

RESULTS: Eleven patients were diagnosed as IGP. Nine had active EV infection on gastric biopsies and were included (7/9 female, mean age 43 years). Eight out of nine received EV treatment with antivirals and/or immune therapies, with a wide degree of variability in treatment regimens. Four out of eight who received EV treatment had symptomatic improvement. One patient had stable symptoms. Three patients are currently undergoing therapy.

CONCLUSIONS: Gastric EV infection was frequently detected (82 %) in patients undergoing investigation for IGP. Antiviral and/or immune therapies against EV seem to be favorable, as most of our patients had resolution of their GP symptoms after treatment. This is the first study to identify EV as a possible infectious etiology of IGP.

Gastric Enterovirus Infection: A Possible Causative Etiology of Gastroparesis. by Barkin JA, Czul F, Barkin JS, Klimas NG, Rey IR, Moshiree B. in Dig Dis Sci. 2016 Jun 25. [Epub ahead of print]

Posted in News | Tagged , , | Comments Off on Gastric enterovirus infection: a possible cause of gastroparesis

Indicator of CFS found in gut bacteria

Posted on 06/27/2016 by wames

Cornell Chronicle blog post by Krishna Ramanujan, 24 June 2016: Indicator of chronic fatigue syndrome found in gut bacteria

Physicians have been mystified by chronic fatigue syndrome, a condition where normal exertion leads to debilitating fatigue that isn’t alleviated by rest. There are no known triggers, and diagnosis requires lengthy tests administered by an expert.

Due to this lack of information, some people have even suggested the disease may be psychosomatic.

Now, for the first time, Cornell researchers report they have identified biological markers of the disease in gut bacteria and inflammatory microbial agents in the blood.

In a study published June 23 in the journal Microbiome, the team describes how they correctly diagnosed myalgic encephalomyeletis/chronic fatigue syndrome (ME/CFS) in 83 percent of patients through stool samples and blood work, offering a noninvasive diagnosis and a step toward understanding the cause of the disease.

“Our work demonstrates that the gut bacterial microbiome in ME/CFS patients isn’t normal, perhaps leading to gastrointestinal and inflammatory symptoms in victims of the disease,” said Maureen Hanson, the Liberty Hyde Bailey Professor in the Department of Molecular Biology and Genetics and the paper’s senior author. “Furthermore, our detection of a biological abnormality provides further evidence against the ridiculous concept that the disease is psychological in origin.”

Ruth Ley, associate professor in the Departments of Molecular Biology and Genetics and Microbiology, is a co-author.

“In the future, we could see this technique as a complement to other noninvasive diagnoses, but if we have a better idea of what is going on with these gut microbes and patients, maybe clinicians could consider changing diets, using prebiotics such as dietary fibers or probiotics to help treat the disease,” said Ludovic Giloteaux, a postdoctoral researcher in both Hanson’s and Ley’s labs and first author of the study.

Researchers have evidence that an overactive immune system plays a role in chronic fatigue. Symptoms include fatigue even after sleep, muscle and joint pain, migraines and gastrointestinal distress. One hallmark of the condition is post-exertional malaise, meaning patients may take weeks to recover from minor exertion. To test for ME/CFS, clinicians may give patients a cardio-pulmonary exercise test where they ride a bike until they become fatigued. If the test is repeated the following day,  ME/CFS patients usually cannot reproduce their performance from the first day.

“That’s very typical and specific of people with ME/CFS, because healthy people, or even people who have heart disease, can reproduce the exercise on the second day, but these people cannot,” Giloteaux said.

In the study, Ithaca campus researchers collaborated with Dr. Susan Levine, an ME/CFS specialist in New York City, who recruited 48 people diagnosed with ME/CFS and 39 healthy controls to provide stool and blood samples.

The researchers sequenced regions of microbial DNA from the stool samples to identify different types of bacteria. Overall, the diversity of types of bacteria was greatly reduced and there were fewer bacterial species known to be anti-inflammatory in ME/CFS patients compared with healthy people, an observation also seen in people with Crohn’s disease and ulcerative colitis.

At the same time, the researchers discovered specific markers of inflammation in the blood, likely due to a leaky gut from intestinal problems that allow bacteria to enter the blood, Giloteaux said.

Bacteria in the blood will trigger an immune response, which could worsen symptoms.

The researchers have no evidence to distinguish whether the altered gut microbiome is a cause or a whether it is a consequence of disease, Giloteaux added.

In the future, the research team will look for evidence of viruses and fungi in the gut, to see whether one of these or an association of these along with bacteria may be causing or contributing to the illness.

Co-authors include Julia Goodrich, a doctoral student, and William Walters, a postdoctoral researcher, both in Ley’s lab.

The study was funded by the National Institutes of Health.

Reduced diversity and altered composition of the gut microbiome in individuals with myalgic encephalomyelitis/chronic fatigue syndrome by Ludovic Giloteaux, Julia K. Goodrich, William A. Walters, Susan M. Levine, Ruth E. Ley and Maureen R. Hanson in Microbiome 2016 4:30 [published 23 June 2016]

Posted in News | Tagged , , , , , , | Comments Off on Indicator of CFS found in gut bacteria

Research project to evaluate daily activity patterns and heart rate

Posted on 06/25/2016 by wames

Newswise Stony Brook University blog post, by …, 23 June 2016: Getting to the Heart of Chronic Fatigue Syndrome

Stony Brook researcher receives $1.5 million NIH grant to evaluate daily activity patterns and heart rate of those who suffer from this debilitating illness

By better understanding daily activity levels and heart rate patterns of those who suffer from Chronic Fatigue Syndrome (CFS), scientists hope to discover more about this complex illness condition. Fred Friedberg, PhD, Associate Professor of Psychiatry at Stony Brook University School of Medicine, has received a four-year $1.5 million grant from the National Institutes of Health to take this research approach to determine if heart rate fluctuations in combination with certain daily activity patterns can be used to predict or prevent relapse in people with CFS.

According to Dr. Friedberg, also the President of the International Association for Chronic Fatigue Syndrome/Myalgic Encephalomyelitis, CFS affects some one million people in the United State and millions worldwide. This condition is characterized by a state of chronic fatigue and other debilitating symptoms, such as post-exertional collapse and cognitive difficulties. These symptoms and related impairments persist for more than six months and have no clearly identified cause.

This study will involve patients self-reporting their symptoms and activities on a weekly online diary over a period of six months. Data will also be recorded from mobile heart devices and activity monitors that the patients wear at home. Over the six month study period, patients will regularly send this objective data back to the Stony Brook laboratory where the information will be downloaded and analyzed for patterns related to CFS symptoms, activities, and impairments. The participants will then be interviewed by a psychiatric nurse via phone about other potentially important illness factors including major life events they have experienced over the study period, their physical and social functioning, and changes in their illness status – i.e., improved or worsened.

“What is promising is that we have proposed an illness model to potentially identify the factors that lead to relapse or improvement,”  said Dr. Friedberg. “If a predictor of relapse is discovered, such as heart rate variability in conjunction with certain activity patterns, we may be able to prevent or reduce relapse by adjusting such activity patterns in advance. This could potentially be the first biomarker of illness worsening or improvement in this illness.”

Dr. Friedberg expects that the data collected from the study will be used to generate a new, potentially more effective self-management program that ultimately helps patients avoid relapses and feel and function better.

About Stony Brook University
Part of the State University of New York system, Stony Brook University encompasses 200 buildings on 1,450 acres. Since welcoming its first incoming class in 1957, the University has grown tremendously, now with more than 25,000 students and 2,500 faculty.
Its membership in the prestigious Association of American Universities
(AAU) places Stony Brook among the top 62 research institutions in North America. U.S. News & World Report ranks Stony Brook among the top 100 universities in the nation and top 40 public universities, and Kiplinger names it one of the 35 best values in public colleges. One of four University Center campuses in the SUNY system, Stony Brook co-manages Brookhaven National Laboratory, putting it in an elite group of universities that run federal research and development laboratories. A global ranking by U.S. News & World Report places Stony Brook in the top 1 percent of institutions worldwide. It is one of only 10 universities nationwide recognized by the National Science Foundation for combining research with undergraduate education. As the largest single-site employer on Long Island, Stony Brook is a driving force of the regional economy, with an annual economic impact of $4.65 billion, generating nearly 60,000 jobs, and accounts for nearly 4 percent of all economic activity in Nassau and Suffolk counties, and roughly 7.5 percent of total jobs in Suffolk County.

Posted in News | Tagged | Comments Off on Research project to evaluate daily activity patterns and heart rate

CFS following low-level radiation exposure

Posted on 06/24/2016 by wames

2 articles about the effects of low-level radiation are on the National CFIDS Foundation website at

Health of Liquidators (Clean-up Workers) 20 Years after the Chernobyl explosion

Chronic Fatigue Syndrome is one of the most important consequences of radioecological disaster resulting in an interaction of different hazardous environmental factors. CFS can be considered as an environmentally induced predisposition and vestige of forthcoming neurodegeneration that included cognitive impairment.  Increased incidence of CFS has been seen in exposed populations in Chernobyl, Hiroshima and Nagasaki.

Health Effects of Chernobyl and Fukushima: 30 and 5 years down the line

The article was commissioned by Greenpeace of Belgium.

A prospective study of personnel working on transformation of the Chernobyl NPP Object “Shelter” into an ecologically safe system showed that exposure to radiological (0–56.7 mSv, М±SD:19.9±13.0 mSv dose) and industrial risk factors may lead to the onset of cognitive CFS characterized by a dysfunction of cortical-limbic system mainly in the dominant (left) hemisphere with an important involvement of hippocampus. page 45

Posted in News | Tagged , , , | Comments Off on CFS following low-level radiation exposure

PACE trial cost-effectiveness conclusions faulty

Posted on 06/24/2016 by wames

Health rising blog post, by Cort Johnson, 31 May 2016: Another Ball Drops in PACE Controversy: Cost-effectiveness Conclusions Faulty – Plus Update

Some past efforts to clear up the controversies around the now notorious PACE trials have requested that the authors release the raw data to researchers to be re-analyzed. Not so this time. In the latest ball to drop for the PACE studies, MEAction reported that five researchers including Ron Davis, two biostatisticians and an epidemiologist requested that the PLOS One Journal simply delete a finding they assert the papers own figures indicate is incorrect.

The paper in question is “Adaptive Pacing, Cognitive Behaviour Therapy, Graded Exercise, and Specialist Medical Care for Chronic Fatigue Syndrome: A Cost-Effectiveness Analysis.”

The finding is not a minor one. It asserts that the authors conclusion that the CBT/GET protocols used in the study were, from a societal perspective, cost/effective was incorrect. One of the main goals of the PACE Trial, was to demonstrate to the UK government and other funding bodies that they would get the most bang from their buck with ME/CFS by employing CBT/GET.

The PACE trial protocols called for sensitivity analyses that examined cost-effectiveness from a several scenario’s including CBT/GET’s ability to reduce the amount of home care provided by professional home care providers or by family members either paid a minimum wage or no wages.

The paper report that the societal benefits outweighed the costs of CBT/GET under any of these scenario’s was inaccurate. CBT/GET was only determined to be cost-effective from a societal perspective if the authors treated family caregivers as if they being paid as if they were home care providers. Under the other scenario’s it was not. It was another case of the authors stretching their findings beyond the breaking point.

As with other instances patient advocates played a major role in getting the word out about PACE trial problems.

Simon McGrath,Tom Kindlon and other ME/CFS advocates took the authors to task regarding a number of their conclusions. Using figures from one of the CBT/GET centers used in the trial Kindlon demonstrated that the PACE authors underestimated the cost of GET treatments by as much as 300% (if I’m reading it correctly). At that cost of treatment the CBT/GET doesn’t begin to pay for the advantages it provides.

The Davis paper simply asks that the paper be changed to reflect what Davis and other believe the authors have already admitted; that only if you treat the value of family members time as if they were paid home care providers, do the conclusions make any sense.

PACE Controversy Update

The Lancet Study – Over ten studies have emanated from the PACE trial thus far. The first was published in The Lancet; one of the oldest and most prestigious medical journals in the world. In Nov. 2015 Ron Davis, Lenny Jason, Vincent Racaniello and others posted a open letter to Lancet asking that independent analyses of the PACE trial be redone using outside researchers.

We therefore urge The Lancet to seek an independent re-analysis of the individual-level PACE trial data, with appropriate sensitivity analyses, from highly respected reviewers with extensive expertise in statistics and study design. The reviewers should be from outside the U.K. and outside the domains of psychiatry and psychological medicine. They should also be completely independent of, and have no conflicts of interests involving, the PACE investigators and the funders of the trial.

Horton replied that he was traveling and would get to the issue. Three months later after Horton had still not replied another letter went out with three dozen more signatories. It’s now six months later and Horton has still not replied.

The PLOS Study – The complaints began soon after the present paper was published in 2012. In Dec. 2015 PLOS stated that it expected the study authors to share the study data, and that they were doing their own internal investigation using outside experts to help them evaluate the issues.

In March, 2016 PLOS stated they had determined which data they believed should be shared and had requested the authors share it.

University – Jennie Spotila reported that the University sponsoring the study refused, citing the privacy needs of the participants and “prejudice to the programme”, to provide the raw study data (was it not anonymized?) to Vincent Racaniello and others. An appeal has been filed.

Conclusion

The PACE trial authors and the journals publishing their studies appear to be engaged in a waiting game in hopes the controversy will simply disappear over time. Until that happens they are ignoring requests or simply ignoring major issues.

David Tuller has tried and failed to have substantive, or in most cases, any conversations with the PACE trial authors. He and others have also contacted the journals the papers were been published in. When they do go on record – which is rare – Tuller reports they are evasive and provide misleading answers.

An investigative reporter of long standing Tuller has seen a lot, but even he seems taken aback by the unwillingness of the PACE authors or their publishers to address the legitimate issues that have been raised.

They appeared to excel at avoiding hard questions, ignoring inconvenient facts, and misstating key details. I was surprised and perplexed that smart journal editors, public health officials, reporters and others accepted their replies without pointing out glaring methodological problems—such as the bizarre fact that the study’s outcome thresholds for improvement on its primary measures indicated worse health status than the entry criteria required to demonstrate serious disability.

Jenny Spotila reported that Racaniello has little faith in the journals doing the right thing:

“I think they are going to ignore, obfuscate, and give their usual responses until we are all dead. I don’t have hope that the PACE authors, or Lancet, will respond in any meaningful way until there is more of an outcry.” Vincent Racaniello

The battle is not over by an means, however. The key to getting Lancet and the other publishers to act is simply getting more researchers to join in the fray and keeping the pressure on.

Posted in News | Tagged , , , | Comments Off on PACE trial cost-effectiveness conclusions faulty

Circulatory Impairment in ME

Posted on 06/23/2016 by wames

ME Advocacy Blog post extract, 14 June 2016: Circulatory Impairment in Myalgic Encephalomyelitis: A Preliminary Thesis, by Maryann Spurgin, Ph.D.

Here is my proposal:
For many years, I have followed and collated research on Myalgic Encephalomyelitis (ME), in particular on the circulatory impairment of which Dr. A. Melvin Ramsay spoke and of which there are many recently discovered facets. Despite lack of research on circulatory impairment in ME in the 1950’s, Dr. A. Melvin Ramsay astutely observed it clinically as one of the three essential components of ME, noting pale, cold skin as a sign.

Sixty years later, the research behind these observations is now extensive, although some of that research was published under the name “CFS”; yet it applies to patients with ME or those with ME who are misdiagnosed with “CFS,” itself a govt construct that, as noted above, has impeded consistent findings. My view is that “CFS” is a government construct.

There are people with everything from MS to fibromyalgia to depression to ME who are diagnosed with “CFS.” So there are not two separate diseases, ME and “CFS”; rather, those diagnosed with “CFS” have something else in need of diagnosis, whether ME or another disease. Much of the research on ME was done under the name “CFS.”

I have spent 22 years studying circulatory impairment in ME by reading published research on its many facets, beginning over 20 years ago with Dr. L.O. Simpson’s work on impaired capillary blood flow [1], the haematological/ hemorheological flow problems that impede delivery of oxygen and nutrients to organs and tissues and impede removal of lactic acid, toxins and metabolic waste due to poorly deformable Red Blood Cells.

Much later, in the 1990’s, Dr. David Bell’s and the late Dr. David Streeten’s joint work on low blood volume (hypovolemia) in ME was published [2, 3]. Dr. Streeten was a world-renowned endocrinologist whose area of specialization was blood pressure and orthostatic disorders.

The third aspect of circulatory impairment is cardiac:

The late Dr. A. Martin Lerner pioneered it, with his hypothesis that the disease is a viral cardiomyopathy. He found on biopsies virally infected cardiac myocytes in the disease, published in the 1990’s [4-6]. He argued that the disease is at its root a viral cardiomyopathy.

Importantly, there was also NIH grant-funded research by Drs Benjamin Natelson and Arnold Peckerman on abnormal impedance cardiography and other cardiac abnormalities in ME patients [7]. These important studies influenced researcher/clinician Dr. Paul Cheney, who found and illuminated problems with cardiac diastolic dysfunction in the disease (diastolic problems not caused by volume depletion but by a pathology in the heart itself), following his own experience with heart failure and his subsequent heart transplant.

This extensive body of research shows that, without identifying the root cause of ME, disorders of microcirculation and macrocirculation are well established pathophysiological findings [8-11], and that combined circulation problems can conspire to create havoc in the heart and other organs of the body.

I have thought a lot about circulatory problems over many years, and how these impairments come together to create the intolerable symptomatology of ME that could lead someone to be so impaired as to not be able to swallow, and could lead the Institute of Medicine to declare that organ failure, even death, can occur from the slightest exertion and/or sensory overload.

This happens, I believe, when one or more or all of the following three conditions hold:

  1. Metabolic demand exceeds the capacity for cardiac output. Studies have shown that if the level of exertion or metabolic demand on the heart exceeds the capacity of the heart to pump blood by even 1%, the organism dies. Rest and limiting demands on a heart whose output is reduced by disease is crucial to survival.
  2. An impaired RBC/capillary delivery system is present (My own theory is that this impairment may be a defense mechanism to slow metabolic demand in order to protect the heart); And…
  3. When low blood volume is present.

One of these impairments alone could cause havoc, but the three of these pathophysiologies together could lead to extreme multisystem involvement and death. In a patient who is already volume depleted, poor diastolic filling from still another, cardiac problem could be doubly dangerous, yet this is exactly what Dr. Cheney has found.

Although this research does not hypothesize a cause, and circulation problems are likely the result of some underlying (likely viral) cause, this particular aspect of the pathophysiology, I believe, is crucial to a biological understanding of ME, and to explaining why ME patients relapse and can die from exertion. Mitochondrial problems that are not primary mitochondrial disease but are an epiphenomenon of the (unknown) cause or causes likely also play a role, especially in cardiac and brain dysfunction (see the home page of my website that discusses mitochondrial epiphenomena and the references I provided on the site).

 

Posted in News | Tagged , , , , | Comments Off on Circulatory Impairment in ME