Estimating the disease burden of ME/CFS in the US

Posted on 01/19/2017 by wames

Article abstract:

At the National Institutes of Health (NIH), burden of disease is an important factor in funding decisions along with such factors as scientific opportunity, the quality of the science, and the interest of researchers.

Recent studies have quantified the burden for a number of diseases in the United States and the NIH has used that information to analyze how its own funding patterns correspond to disease burden. However, the burden of disease has not been quantified for myalgic encephalomyelitis, also called chronic fatigue syndrome (ME/CFS) and is often underestimated due to a lack of research and the misperceptions about the nature of the disease.

Using the limited information in the literature, this paper develops a preliminary estimate of the disease burden of ME/CFS in the United States, using the World Health Organization’s Disability Adjusted Life Years (DALY) measure. The ME/CFS DALY estimate is then compared to the NIH’s 2013 analysis of research funding versus DALY across other funded diseases in order to estimate a level of funding for ME/CFS that would be commensurate with disease burden.

Even given the limitations arising from sparse data, this analysis demonstrates that federal research funding for this disease is far less than what would be expected by the burden of the disease.

We conclude that the annual research funding for ME/CFS would need to increase twenty-five fold or more to be commensurate with disease burden. This level of funding would best leverage the growing interest of researchers and the significant scientific opportunities that exist to understand the pathology of this disease and to advance diagnostics and treatments.

Estimating the disease burden of ME/CFS in the United States and its relation to research funding, by Mary. E. Dimmock, Arthur A. Mirin, Leonard A. Jason in the Journal of Medicine and Therapeutics (new open access journal), 9 December 2016.

See also:

ME Action blog post: Dimmock, Mirin & Jason: Estimating disease-burden in the US

 

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A systematic review of the association between fatigue & genetic polymorphisms

Posted on 01/18/2017 by wames

Review abstract:

Fatigue is one of the most common and distressing symptoms, leading to markedly decreased quality of life among a large subset of patients with a variety of disorders. Susceptibility to fatigue may be influenced by genetic factors including single nucleotide polymorphisms (SNPs), especially in the regulatory regions, of relevant genes.

To further investigate the association of SNPs with fatigue in various patient populations, a systematic search was conducted on Pubmed, CINAHL, PsycINFO, and Sociological Abstracts Database for fatigue related-terms in combination with polymorphisms or genetic variation-related terms.

Fifty papers in total met the inclusion and exclusion criteria for this analysis. These 50 papers were further classified into three subgroups for evaluation: chronic fatigue syndrome (CFS), cancer-related fatigue (CRF) and other disease-related fatigue.

SNPs in regulatory pathways of immune and neurotransmitter systems were found to play important roles in the etiologies of CFS, CRF and other disease-related fatigue. Evidence for associations between elevated fatigue and specific polymorphisms in TNFα, IL1b, IL4 and IL6 genes was revealed for all three subgroups of fatigue.

We also found CFS shared a series of polymorphisms in HLA, IFN-γ, 5-HT and NR3C1 genes with other disease-related fatigue, however these SNPs (excluding IFN-γ) were not found to be adequately investigated in CRF. Gaps in knowledge related to fatigue etiology and recommendations for future research are further discussed.

A systematic review of the association between fatigue and genetic polymorphisms, by Wang T, Yin J, Miller AH, Xiao C in Brain Behav Immun. 2017 Jan 12 pii [Epub ahead of print]

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Children’s experiences of CFS/ME

Posted on 01/18/2017 by wames

Review abstract:

Objective:
To synthesis the qualitative studies of children’s experiences of chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME).

Design:
Systematic review and meta-ethnography.

Background:
CFS/ME is an important disabling illness, with uncertain cause and prognosis. As a result, children with CFS/ME can find themselves living with greater uncertainty and stigma, exacerbating the impact of the condition. There is a growing body of qualitative research in CFS/ME, yet there has been no attempt to systematically synthesis the studies
involving children.

Methods:
Studies exploring the experiences of children diagnosed with CFS/ME, published or unpublished, using qualitative methods were eligible.  MEDLINE, EMBASE, PsycINFO and CINAHL databases were searched as well as  grey literature, reference lists and contacting authors. Quality assessment was done independently using the Critical Appraisal Skills Programme (CASP) checklist. Studies were synthesised using techniques of meta-ethnography.

Results:
Ten studies involving 82 children with CFS/ME aged 8-18 were included. Our synthesis describes four third-order constructs within children’s experiences: (1) disruption and loss: physical, social and the self; (2) barriers to coping: suspension in uncertainty, problems with diagnosis and disbelief; (3) facilitators to coping: reducing uncertainty,
credible illness narratives, diagnosis and supportive relationships and (4) hope, personal growth and recovery. CFS/ME introduces profound biographical disruption through its effects on children’s ability to socialise, perform school and therefore how they see their future.

Unfamiliarity of the condition, problems with diagnosis and felt stigma prevent children from forming a new illness identity. Children adopt coping strategies such as building credible explanations for their illness.

Conclusions:
Physical, social, emotional and self-dimensions of life should be included when treating and measuring outcomes from healthcare in paediatric CFS/ME. There is a need for greater recognition and diagnosis of childhood CFS/ME, specialist advice on activity management and improved communication between health and education providers to help children cope with their condition.

Strengths and limitations of this study

  • To the best of our knowledge, this is the first systematic review and meta-ethnography of the qualitative literature of children’s experiences of chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME).
  • We included all published and unpublished studies from any language to avoid bias.
  • The synthesis of studies from multiple contexts identified the main dimensions of life impacted, as well as barriers and facilitators to living with childhood CFS/ME.
  • The findings from this synthesis could be used to inform healthcare practice and the development of outcome measures in paediatric CFS/ME.
  • The majority of studies were conducted in western countries reducing the transferability of findings.

Children’s experiences of chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME): A systematic review and meta-ethnography of qualitative studies, by Roxanne M Parslow, Sarah Harris, Jessica Broughton, Adla Alattas, Esther Crawley, Kirstie Haywood, Alison
Shaw in BMJ Open 2017:7

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Discussion of Fluge’s finding of key metabolic enzyme impairment in ME/CFS

Posted on 01/18/2017 by wames

TV2 interview with Dr Øystein Fluge on his latest research on ME/CFS – in Norwegian with English subtitles. Begins with a man who is very severely affected by ME.
(11 minutes 23 seconds)    Watch video

 

Medscape Medical news article, 13 January 2017: Possible mechanism identified for ‘Chronic Fatigue Syndrome’, by Miriam E. Tucker 13 January 2017

Blockage of a key metabolic enzyme could explain the profound lack of energy and other symptoms experienced by patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), new research suggests.

The findings were published December 22, 2016, in the Journal of Clinical Investigation Insight by Øystein Fluge, MD, from the Department of Oncology and Medical Physics at Haukeland University Hospital, Bergen, Norway, and colleagues.

The study included 200 patients with ME/CFS, as defined by the 2003 Canadian Consensus Criteria, which requires the hallmark symptom of postexertional malaise, among others, to make the diagnosis of ME/CFS.

The authors compared serum concentrations of 20 standard amino acids from the 200 patients with ME/CFS and 102 healthy control patients.

In the patients with ME/CFS, there was a specific reduction of amino acids that fuel oxidative metabolism, pointing to functional impairment of pyruvate dehydrogenase (PDH), a key enzyme for the conversion of carbohydrates to energy. Impairment of PDH could result in the cells switching to consumption of alternative fuels, causing a sudden shortage of energy in the muscles and a buildup of lactate, experienced by patients as a burning sensation in their muscles after even minor exertion.

“I think that at present our data are primarily telling us something about the ME/CFS disease. Our findings indicate an impaired function of the PDH enzyme complex, resulting in reduced flux of pyruvate to the [tricarboxylic acid (TCA)] cycle. Increased lactic acid accumulates upon limited exertion, and there is a compensatory use of alternative substrates to fuel the TCA cycle. So, the results indicate an impaired mitochondrial PDH complex function, we believe induced by the immune system,” Dr Fluge told Medscape Medical News.

The model, if correct, has implications for prescribing exercise for patients with ME/CFS.

“Based on the findings in the study, we can understand why patients need to stay at rest, minimizing the energy deficiency and reducing the symptoms caused by lactic acid accumulation…. The value of doing exercise should, however, not be underestimated, and the level of activity tolerated will depend on the severity of the disease,” Dr Fluge said.

He added, “An ME/CFS patient’s ability to handle exercise is very individual. Generally, I think the physicians should listen carefully to the patients, and find the optimal activity level through pacing, to avoid ‘crashing’ with the resulting major symptom increase that can last for weeks and months.”

Asked to comment, Anthony L. Komaroff, MD, professor of medicine at Harvard University, Boston, Massachusetts, and editor-in-chief of the Harvard Health Letter, told Medscape Medical News,

“This is the latest of many research studies that are pursuing a simple idea: That the human being who says ‘I don’t have enough energy’ could have a problem with their cells producing enough energy…. It adds to a large literature indicating that cellular energy metabolism is abnormal in patients with ME/CFS.”

However, he cautioned that the investigators inferred the abnormality in PDH, rather than directly measuring it, and that although “[t]heir argument seems plausible…I wouldn’t be convinced until a second study by other investigators, studying other patients with ME/CFS, confirmed this.”

Dr Komaroff also said, “What is urgently needed are some testable hypotheses that would explain the several different reported abnormalities in energy metabolism [in ME/CFS].”

Read more:  the article goes on to discuss the different results found between women and men, and the argument against the involvement of deconditioning in energy impairment.

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Myhill & McLaren-Howard discuss apparent contradictions in mitochondria research

Posted on 01/17/2017 by wames

DoctorMyhill.co.uk article, by Dr Sarah Myhill & John Howard-McLaren-Howard, 11 January 2017: Reply to Lawson Paper

Background:

In 2016, Nick Lawson, Chung-Han Hsieh, Dana March, Xinnan Wang published a paper with the title “Elevated Energy Production in Chronic Fatigue Syndrome Patients” in the Journal of Nature and Science (J Nat Sci 2016; 2(10):e221. The full paper can be viewed here:

“Elevated Energy Production in Chronic Fatigue Syndrome Patients” Nick Lawson, Chung-Han Hsieh, Dana March, and Xinnan Wang

At first sight, the conclusions of this paper may seem to be at odds with the three papers that I have co-authored on mitochondrial dysfunction.

Lawson et al conclude that:

“To thoroughly reveal mitochondrial deficiencies in CFS patients, here we examine the key aspects of mitochondrial function in blood cells from a paired CFS patient-control series. Surprisingly, we discover that in patients the ATP levels are higher……”

This compares with the conclusion that Professor Norman E. Booth, Dr John McLaren-Howard and I came to in our first published paper, “Chronic fatigue syndrome and mitochondrial dysfunction”:

“Our observations strongly implicate mitochondrial dysfunction as the immediate cause of CFS symptoms.”

Our first published paper can be found here – “Chronic fatigue syndrome and mitochondrial dysfunction”

This conclusion of impaired energy production in CFS patients was supported by our two subsequent papers which can be found as below:

I explain these ideas in more detail on my webpage – CFS – The Central Cause: Mitochondrial Failure

Explanation of this apparent conflict:

Dr John McLaren-Howard has produced the note below to explain this apparent conflict. The note is reproduced in full with John’s permission.

Full text of John McLaren-Howard note:
On initial perusal of the title, the following paper may initially seem to be a contradiction of our test findings in CFS/ME patients. However, closer examination of the contents of this publication leads to some very important possibilities.

Ref: Nick Lawson, Chung-Han Hsieh, Dana March, Xinnan Wang. Elevated Energy Production in Chronic Fatigue Syndrome Patients. J Nat Sci 2016; 2(10):e221

The authors conclude that CFS/ME patients have higher ATP levels that controls. Their work was done on cultured cells while all of our test data is on the patients’ cells as separated from a whole-blood sample. So why the difference?

About 35% of our abnormal ATP-profiles show chemical blocking of ADP to ATP re-conversion at the translocator (TL) sites of the inner mitochondrial membranes and over 90% show poor ADP to ATP re-conversion even if TL-sites are not apparently blocked. This presumably reflects other problems with the electron-transport chain (oxidative phosphorylation). That could include chemical or metabolic blocking of one-or-more of the enzyme complexes.

If the ATP levels are measured on cultured cells the effect of any blocking agent may be negated. For argument’s sake, let’s take a situation where 20% of the TL sites are blocked by a chemical we will call X. If the cells are cultured the ‘new’ cells will be unaffected by the blocking agent X which is not itself cultured: X probably being an environmental chemical, drug or metabolic biochemical. In our hypothetical example, when in the culture 10 times the original cell number is reached only 2% would be affected by X. When a very moderate amplification of 100 times the cell numbers is reached only 0.2% of the cells would be affected by X etc etc…………

The changes we see in terms of the blocking of TL sites and other chemical interferences are negated when cultured cells are used to assess ATP metabolism in CFS/ME patients. That being the reason why I rejected the use of cultured cells during the development of the ATP-profile performed here.

BUT, this paper does reflect exciting work. It demonstrates the ability of the ‘new’ cells to produce increased levels of ATP. This supports what many doctors have reported to me and what has been my own experience. When steps are taken to eliminate blocking chemicals, whether affecting TL sites or interfering with steps in the electron-transport chain, and/or substrate deficiencies are addressed, there are almost always clinical improvements. These can be dramatic, moderate, but very welcome by the patients, and sometimes only mild. In the latter cases there is clearly more to learn although it often pivots on renewed individual assessment rather than some as yet unknown scientific area.

I am very grateful to the authors of the above paper for their work and contribution although I could wish they had chosen a different title in order to avoid confusion.

If I can find the time I will carry out some comparisons between the ATP in cells directly from CFS patients and in the cultured cells. It would be of even greater value if this was assessed by a third party laboratory.”

Pheonix rising forum post, 21 Oct 2016: Mitochondrial and Energy Metabolism Dysfunction in ME/CFS — Myhill, Booth and McLaren-Howard Papers 

The ME/CFS Energy Metabolism Studies of Dr Sarah Myhill et al – a discussion of the three very incisive studies of Dr Sarah Myhill, Norman E. Booth and John McLaren-Howard (published in 2009, 2012 and 2013) on the dysfunctional energy metabolism of ME/CFS.

  • Dr Sarah Myhill is a GP with a great deal of research interest and expertise in treating ME/CFS.
  • Dr Norman E. Booth is a retired academic physicist with two family members who have been affected by ME/CFS.
  • Dr John McLaren-Howard is cofounder of Biolab Medical Unit, and medical director of Acumen Labs, UK.
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Is mitochondrial function abnormal in ME/CFS?

Posted on 01/17/2017 by wames

ME Research UK article, 12 January 2017: Is mitochondrial function abnormal?

Mitochondria are often referred to as the power plants of the body because they are responsible for generating nearly all the energy needed to support life.

These kidney bean-shaped structures are found in most cells and are made up of different compartments, each with a specific role related to the metabolism of the cell they inhabit.

One of these roles is the generation of adenosine triphosphate (ATP), a molecule that is used to transport energy within a cell and thereby enable it to function properly (for example, allowing a muscle fibre to contract).

It is not surprising, therefore, that scientists have considered whether abnormalities in the mitochondria might be involved in ME/CFS, an illness characterised by a loss of muscle power following exertion, which may be due to insufficient energy within the muscle cells.

We have reported on several such studies over the last few years (from the Netherlands, Spain and the UK), but the overall picture is still not clear. Some studies have shown reduced concentrations of ATP in ME/CFS patients, while others have not.

Adding to this story (but not yet making it much clearer) is new research published in the Journal of Nature and Science. US researchers at Stanford and Columbia took blood samples from 42 ME/CFS patients and 42 healthy people in five different clinics, including the Levine Clinic and Sierra Internal Medicine. Their main aim was to look for defects in the structure or function of the mitochondria that might explain some of the symptoms of ME/CFS.

Overall, the researchers found no difference in the density, size or shape of mitochondria in patients, nor in several other aspects of their structure and function, although the cristae (protrusions of the membranes inside the mitochondria) were more condensed than usual.

They did find that ATP levels were higher than normal in the blood samples from ME/CFS patients. Further testing showed that the mitochondrial production of ATP was actually relatively normal, suggesting that the extra ATP was being generated elsewhere.

The main conclusion of the study, however, was that there were no major abnormalities in the mitochondria of ME/CFS patients: the important parts of this structure were all intact and functioning, and ATP production was normal.

It is important to note that these measurements were made in mitochondria from blood cells, and it is possible that the situation in muscle cells is quite different. But at least one study that did look at muscle mitochondria has also reported normal ATP production.

If the muscle fatigue in ME/CFS is not a result of a lack of mitochondrial ATP, then what is the cause? We still don’t know, but the intriguing hypothesis suggested by these researchers is that there is some pathological process occurring by which extra ATP is being produced somewhere else. And the scientists’ next step is to identify where and why this is happening.

 

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PACE trial data assessment: in ME/CFS CBT and GET are ineffective

Posted on 01/17/2017 by wames

Research abstract:

The PACE trial concluded that Cognitive Behavioral Therapy (CBT) and Graded Exercise Therapy (GET) are moderately effective in managing Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and yielded a 22% recovery rate.

Nonetheless, the recently released individual participant data shows that 13.3% of patients had already recovered, on one or both primary outcomes, upon entering the trial. Moreover, no one classified as recovered achieved the physical functioning, together with the fatigue scores, of the healthy sedentary controls from another trial by the PACE trial‘s lead principal investigator or achieved Kennedy‘s definition of recovery, whereby symptoms are eliminated and patients return to premorbid levels of functioning, due to CBT or GET (alone).

Therefore, CBT and GET do not lead to actual recovery. After CBT and GET therapy, 59% and 61% of participants, respectively were labeled as improvers in the original paper, which was lowered by the PACE trial authors to 20% and 21% in the newly released papers in which they used the original protocol; nevertheless, only 3.7% and 6.3% were objective improvers in the objective 6-minute walk test as defined by the same improvement of 50% or more, as used by the trial itself, to classify someone as an improver.

If the effect of Specialist Medical Care had been removed from the analysis, then 0% and 1.3% of patients improved objectively with CBT and GET, respectively. Highlighting the fact that unblinded trials like the PACE trial, should not rely on subjective primary outcomes, but use either objective primary outcomes alone, or combined with subjective primary outcomes, as a methodological safeguard against the erroneous inference of efficacy in its absence.

The objective individual participant data shows that in up to 82.2% and 79.8% of ME patients their health might have been negatively affected by CBT and GET, respectively. The independent PACE trial review had shown that this proportion was between 46% and 96%, and found to be between 63% and 74% by surveys involving more than 3000 patients by the Norwegian, British, and the Dutch ME Associations.

These data confirm the conclusions of a number of studies that patient health was negatively affected by CBT and GET, including one that found that in 82% of patients with severe ME their symptoms were made worse by GET. Analysis of the individual participant PACE trial data has shown that CBT and GET are ineffective and (potentially) harmful, which invalidates the assumption and opinion-based biopsychosocial model.

Consequently, we should stop using CBT and GET as (compulsory) treatments for ME/ CFS to prevent further unnecessary suffering inflicted on patients by physicians, which is the worst of all harms, yet totally preventable.

Assessment of Individual PACE Trial Data: in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, Cognitive Behavioral and Graded Exercise Therapy are Ineffective, Do Not Lead to Actual Recovery and Negative Outcomes may be Higher than Reported, by Mark Vink in Journal of Neurology and Neurobiology 3:1, 2017 [Published online 10 Jan 2017]

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Inquest into death of person with severe ME in North Wales

Posted on 01/16/2017 by wames

Daily Post article, by Gareth Hughes, 12 January 2017:  Coroner questions bed-blocking at Maelor Hospital after woman accidentally killed herself in A&E

A coroner is to ask what steps are being taken to tackle the problem of  bed-blocking at the Maelor Hospital, Wrexham. John Gittins, the coroner for North Wales East and Central, issued a Regulation 28 notice after hearing the situation was probably worse today than two years ago.

Julie Smith, assistant director for nursing with the Betsi Cadwaladr University Health Board, told an inquest that demand for beds constantly exceeded supply despite various efforts to solve the problem. ‘It is an absolutely massive challenge but we are doing our best to manage the pressure,’ she said.

Mrs Smith was giving evidence at an inquest into the death of mother-of-four Sarah Ann Tyler, who accidentally killed herself in the hospital’s emergency department where she had been on a trolley for about eight hours, having been admitted after taking an
overdose of paracetamol.

Miss Tyler, of Ffordd y Gaer, Bradley, was found unconscious with a ligature made of an ECG cable around her neck in the early hours of February 9, 2015.

The hearing was told that she had been suffering from depression and severe ME (myalgic encephalomyelitis) which had left her bed-bound. In a statement read at the inquest her partner David Millward, who was father to her four children, said she was virtually unable to move and was upset at being unable to care for her children. He said she was convinced that the chronic fatigue, not a mental health issue, was her main problem and she felt she was not receiving the specialist treatment for her condition.

In August, 2014, her son found her with a bungee cord around her neck and on February 9 Mr Millward found her with a phone charger cord around her neck, so called the out-of-hours doctor. In the doctor’s presence she took an overdose of paracetamol and Cocodamol and so she was admitted to the emergency department, where she refused to engage with staff. While lying on the trolley she disconnected her intra-venous drip
several times, claiming it had fallen out.

Senior House Officer Dr Thomas Minton told the inquest: ‘I explained what the risks were but she was not giving me anything back.’ Staff nurse Kate Roberts said that Miss Tyler was under half-hourly observation because of the tablets she had taken and was last seen at about 12.20am. About 15 minutes later she was found hanging and despite attempts to resuscitate her she died the following day.

Mrs Smith, who was involved in the serious incident review following the tragedy, said various steps had been taken as a result. These included psychiatric nurses being involved in assessment at a much earlier stage when a patient who has selfharmed arrives in the emergency department.

‘Two years ago nurses used their own professional judgment,’ she said.

Asked by the coroner whether such an incident was less likely to occur now, Mrs Smith replied: ‘Yes, I believe we have reduced the risk, though the improvements are on-going.’ Mr Gittins said his initial fears regarding observation of patients had been allayed but he remained concerned about the severe problem of finding beds for patients, even though he did not believe it played a part in Miss Tyler’s death.

‘Patient throughput continues to be a problem and perhaps even greater now than it was two years ago. I believe it does create a risk,’ he added. He recorded a conclusion of accidental death on Miss Tyler, a cleaner, as he was not persuaded that she wanted to kill herself as she had taken the action in a place where she could expect to be found.

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Narratives of parents living with a child affected by CFS/ME

Posted on 01/16/2017 by wames

Research abstract:

Background and Aims:
Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) remains a poorly understood condition, shrouded by debate, stigma, and uncertainty. Unsurprisingly, the little available research suggests that caring for a Child or Young Person (CYP) affected by the condition can be extremely challenging.

While the majority of available literature is quantitative in nature, there is some qualitative research examining the impact of having a CYP with CFS/ME on parents. However, there currently appear to be no studies examining the narratives of parents living with a CYP with CFS/ME. Therefore, this research aimed to hear how parents narrate their experiences of living with a CYP affected by CFS/ME, paying attention to how they construct their identity, and the contested condition.

Methodology:
This research drew on a qualitative approach that explored the narratives of the participants. A purposive sample of five parents of CYP affected by CFS/ME (5 mothers) was recruited for a single semi-structured interview. The interviews were audio-recorded, transcribed, and analysed using a narrative approach to explore what participants said and how they narrated their accounts. This was then situated within the social and cultural contexts that shaped them.

Analysis and Findings:
Multiple readings of the narratives allowed me to develop a summary of each individual’s narrative account. These were presented, after which similarities and differences across narratives were considered. Analysis identified six areas of collective focus: ‘stories of onset and diagnosis’, ‘stories of battle’, ‘stories of finding the person/people who can help’, stories of impact’, ‘stories of seeking social support’, and ‘stories of coping and adjustment’.

Participants’ narratives were heavily influenced by dominant societal discourses surrounding CFS/ME and motherhood, and could be seen as a response to these narratives.

Consequently, participants offered particular constructions of the condition, themselves, their CYP, and others that they had come into contact with. These findings are discussed with reference to their potential bearing for clinical practice, strengths and limitations of  the methodology, and directions for future research.

Narratives of parents living with a child affected by Chronic Fatigue Syndrome/Myalgic Encephalomyelitis, by  Rosalind Payne. Phd thesis University of Hertfordshire, June 2016 [Published 5 January 2016] Abstract

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The Brain Initiative: FM & ME/CFS perspective

Posted on 01/13/2017 by wames

Health rising blog post, by Cort Johnson, 8 Jan 2017: The Brain Initiative: a Fibromyalgia and Chronic Fatigue Syndrome (ME/CFS) perspective

In the third of three blogs looking at the research efforts of tomorrow and their potential impact on fibromyalgia and chronic fatigue syndrome (ME/CFS) Health Rising looks at the biggest effort of all: the Brain Initiative.

The Brain Initiative

We’ve always suspected that technology is going to provide the answers for diseases like fibromyalgia (FM) and chronic fatigue syndrome (ME/CFS), and nowhere are technological advances more important or necessary than in the brain. With its 100 billion neurons and 100 trillion connections encased in its difficult to penetrate bone helmet it’s easily the hardest organ to get at and understand – and possibly the most important.

Almost all of the symptoms associated with FM and ME/CFS such as the fatigue, pain, cognitive issues, sleep and stimuli problems could conceivably have their origin in the brain. While brain scans regularly find abnormalities in FM, for instance, they’re not precise enough to tell us which neurons, astrocytes or glial cells are causing the problems in these diseases. Similarly, while magnetic stimulation and other brain stimulation techniques can be helpful they’re still crude techniques that lack the ability to target specific brain cells.

On April 2, 2013, the White House proposed a 10-year project—the BRAIN Initiative (Brain Research through Advancing Innovative Neurotechnologies) – to unlock the mysteries of the brain. This Manhattan style project brought together a roster of experts to “catalyze an interdisciplinary effort of unprecedented scope. After a year of work the group reported a series of goals:

  • To classify all the cells in the brain in order to learn how to tweak what
    To produce a full “connectome” of all the millions of connective circuits in the brain
  • Understanding the electrical and chemical activity each type of neuron in the brain engages in
  • Finding new ways to effect brain activity

New tools need to be developed to succeed at each of these goals. The data gathered will be so immense as to require that new statistical methods be produced to adequately analyze it.

The Brain Initiative started funding projects in 2014. Here are some of its recently funded projects:

FIXING THE BRAIN

Changing Brain Activity – a “magnetothermal toolbox” that will locate and activate specific neurons in the brain – thereby paving the way for more precise ways of stimulating or de-stimulating the brain.

Transcranial Magnetic Stimulation to the Rescue?

  • miniaturized rTMS elements that will alter brain activity more precisely and at deeper levels of the brain
  • combine TMS with MRIs in order to simultaneously stimulate multiple brain regions

Focused…Really Focused Ultrasounds

  • Newer functional ultrasounds that use acoustic signals to measure blood vessel volume, however, put older techniques to shame. They’re about 10x more precise.
  • low intensity ultrasound to regulate the activity of neurons in the brain – “sonogenetics” uses sound waves to do just that.
  • creating gaseous nanovesicles (really, really, really small vesicles) derived from microbes that can be introduced into the brain to view the brain, particularly in its deeper levels.
  • a wearable FUS cap that’s designed to modulate the activity of overactive sensorimotor regions of the brain

Shhh…..A Quiet TMS – an inaudible TMS (a qTMS or quiet TMS) machine that is more tolerable, safer, more precise and even more effective.

A Walk Down Memory Lane Again? – a new brain stimulation procedure called “HF-Stim” to enhance the hippocampal-cortical networks which enable us to have memories.

UNDERSTANDING THE BRAIN

The Inflammation Behind Neuroinflammation – DREADDS ( Designer Receptors Exclusively Activated by Designer Drugs) to determine which kinds of cells are producing neuroinflammation.

Good Vibes – Virtual Brain Electrode project will load red blood cells with magnetic particles in order for researchers to indicate exactly which part of the brain those pathogenic EEG signals are coming from.

fMRI – new technology to tell which kinds of neurons (inhibitory/excitatory) or glial cells are causing problems, which will help determine which kinds of treatment might be best.

Microscopic Resolution – combining fMRIs with other brain imaging technologies to provide three-dimensional maps at the microscopic level of the brain when it is active.

Read more about these projects and how they might benefit people with ME/CFS and FM in the full article at Health Rising.

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