Latest News

August 2018

Having ME Is Like Being Permanently Encased In A Suit Of Armour

https://www.huffingtonpost.co.uk/amp/entry/myalgic-encephalomyelitis-how-it-feels_uk_5b61badbe4b0fd5c73d524cc/

I have, for a long time, struggled to fully get across the impact this illness has on my life

03/08/2018

By Jonathan Davis

I have been asked many times what it is like to have myalgic encephalomyelitis (ME) and I have, for a long time, struggled to fully get across the impact this illness has on my life. To say that I am sick, tired and sore is just too vague. Plus, the condition fluctuates and everyone’s experience of ME is different. But, for me, this is how I would describe what it’s like.

Imagine that you are permanently encased head to toe in a suit of armour. The suit is rusted, stiff, unwieldy and incredibly heavy. Simple tasks like getting out of bed require an enormous effort, even lifting your arms to wash your hair is often too much. Walking around is extremely strenuous causing you to rapidly deplete your glycogen reserves. Within moments you have “hit the wall”. Your muscles shake and cramp, you feel sick and dizzy. If you don’t stop, you will almost certainly collapse. Cruelly, you may feel a sense of accomplishment in your efforts only to look behind you to see you have moved from your chair to the door. Anger and resentment build as you recall how you once took moving with ease for granted. But such intense emotions will rob you of what little precious energy you have left, so you catch yourself, and breathe.

On the inside of the suit of armour are thousands of spikes that press and tear into you whenever you move. Everything you do has to be measured and is carried out with trepidation. The spikes are not clean either so you are constantly fighting infection. Your bones, muscles, and joints ache, your temperature fluctuates wildly. The helmet, instead of protecting you, massively intensifies light and sound. Everyday noises such as the stacking of crockery or a door closing are excruciating and frightening. Light disorientates and burns. You retreat into darkness and silence, where you are isolated, scared and lonely. The outside world is now a painful place to be. In time your home will become a prison; a mausoleum, occupied by a living corpse.

The suit has poisoned your body. Eating causes intestinal discomfort leading to multiple, exhausting and painful trips to the toilet. Your brain is also affected. Words are hard to find. You can’t recall the names of people, even those you are close to, places or everyday items. Conversation is as challenging as a finals exam and reading, even simple text, tests your concentration to the limit. Your short-term memory is poor and you forget important information, constantly having to rely on others for help. Those around you become frustrated because you can’t express yourself or your needs, so you withdraw so as not to be a burden. Lack of interaction reduces your resilience; despair and boredom start to overwhelm you. Your confidence is lost in a sea of self-doubt.

Although your body yearns for rest, there is no refuge in sleep. You are haunted by dreams and nightmares. Even past memories of happy times or achievements are a reminder of what the suit has snatched away from you. What you were once so proud of is now torn to shreds, like a spiteful playground bully destroying a fellow pupil’s prize-winning project.

In such discomfort, you plead with others for help, but there is very little to aid your plight. The suit is invisible to all except you, or others who have similar suits. There is no test yet developed that can detect it and nothing has been proven effective in removing it or mitigating its impact. You draw ire and derision from friends, family, colleagues, and peers who have no knowledge of the suit and what it does to you. Opinion-makers and celebrities mock your condition, even supposed experts in suit-related treatment cast aspersions, abandoning you to your fate. How can you be affected so badly by something that doesn’t exist, they cry, it must all be in your mind.

And yet, every suit of armour has a weakness; in this case, it is knowledge and acceptance. Knowledge through increased funding and medical research and acceptance socially through sharing experiences and education.

ME may be an invisible illness but the people who have it are not.


August 2018

GP system updated to reflect ME as neurological

https://www.actionforme.org.uk/news/gp-system-updated-to-reflect-m.e.-as-neurological/

August 01, 2018

The latest update to the electronic health records system used by GPs in England was launched yesterday, listing M.E. as a neurological disorder. Previously it had sat under two unhelpful and inaccurate headings, mental disorder and multisystem disorder.

The system, SMOMED CT, provides a standard mechanism for recording and collating data across populations which is important for public health monitoring, reporting and analysis as well as influencing decision making. The way it classifies illnesses influences how that illness may be perceived by doctors and other medical professions and others.

Until 2015, CFS (the term SNOMED uses for CFS and/or M.E.) had sat under two headings in SNOMED CT: mental disorder and multisystem disorder, which was clearly unhelpful and inaccurate. Following advocacy efforts made by the Countess of Mar and Forward M.E., the mental disorder heading was retired.

After discussion with Lady Mar, Action for M.E. agreed to take on the role of ‘Coordinator, Classification and Terminology Response Group’ on behalf of Forward M.E.

In February, SNOMED decided to retire the multisystem disorder heading too, leaving CFS (plus around 90 other concepts) without a heading.

With detailed technical advice from long-term SNOMED and ICD-11 advocate, Suzy Chapman, our Chief Executive Sonya Chowdhury contacted SNOMED CT in February to ask that:

  • a new parent term should be assigned given the conflict of classification between SNOMED and various versions of the ICD, the system used by the World Health Organisation (WHO)
  • based on the Institute of Medicine report (2015), CFS (and its related term, M.E.) should be assigned under the heading of Disorder of nervous system parent, until research provides an evidence base for a change.

We are pleased to confirm that this request has been granted, and are hugely grateful to Suzy Chapman, without whom this success would not have been achieved. A more detailed and technical description of how SNOMED classifies illnesses, and the changes made, has been published by Suzy.


July 2018

After the debate – Call for Change

https://www.change.org/p/carol-monaghan-after-the-debate-call-for-change

Call for Change – Submission to the UK Parliament by the international ME/CFS community

The 21st June 2018 saw a truly amazing debate on ME research and treatment in the UK Parliament. Now with real hope for the first time, patients have got together to clearly lay out their hopes for the future, in a Call for Change to the UK government.

The full Call for Change can be viewed and downloaded here, though signatures are still being added and a cover page being designed. Call for Change document

Signatures are invited from the worldwide ME/CFS community. Signing this petition shows your support of the full content of the Call for Change document. Patient organisations may back this Call for Change by emailing your name, website and logo to RColourMusic@hotmail.com.

Let’s unite with a powerful voice that cannot be ignored!

Here is a summary of the outcomes we call for:

1. Stop CBT and GET immediately.

This is most urgent and must be done without any further delay in order to stop further harming patients.

2. A full public enquiry on how ME has been and is being handled in this country.

* The PACE trial and the conduct of its authors, the involvement of the Department for Work and Pensions and the insurance industry.

* The misrepresentation of science through the influence of the PACE authors and proponents of the biopsychosocial model of illness in scientific publications, improperly conducted research and peer review including Cochrane reviews, and the role of scientific journals and their editors.

* The misrepresentation of science through control of the media.

* The unethical use of children in dubious clinical trials of dubious and potentially harmful treatments.

* A close look at the phenomenon of so-called Medically Unexplained Symptoms (MUS) infiltrating our National Health Service, and the new Improving Access to Psychological Therapies (IAPT) programme.

* Examination of the so-called “secret” files on ME/CFS, held by the Medical Research Council and the Department for Work and Pensions in the National Archives at Kew.

* The persecution of doctors who have genuinely tried to help their ME patients with a biomedical approach to the illness.

3. Equivalent funding for biomedical research on ME.

This means stopping inappropriate “research” and having the funds diverted to useful research, providing commensurate funding based on disease prevalence and economic burden, and collaborating with existing important players in biomedical research on ME, such as the charity Invest in ME Research which is already setting up a Centre of Excellence at the Norwich Research Park.

4. Medical Education.

The content of medical education on ME should be developed in collaboration with:

* Practicing ME physicians who take a biomedical approach towards ME.

* Medical professionals who have ME, some of whom also have a background in Medical Education.

* NOT Psychiatrists who call themselves CFS specialists.

5. Appropriate and adequate specialist and community services for ME patients, social support and benefits payments.

* Specialist services should be run by physicians taking a biomedical approach to ME, not Psychiatrists or Mental Health providers.

* Appropriate inpatient care when ME patients are admitted to hospital, appropriately designed nursing home placements where required, and adequate support for the severely ill who live at home, such as with self-care, shopping, cooking, cleaning, and in some cases tube feeding.

* Social welfare assessment that is not only fair to ME patients, but avoids exacerbating their illness and worsening their disability. Assessment protocols and their evidence base should be made available for public scrutiny.

6. Appropriate and adequate care and support for children with ME.

This means correct diagnosis and recognition, and equal access to education. The Department of Health and Department of Education should speak to the UK charity Tymes Trust which has extensive experience in, and in-depth knowledge of, the needs of children with ME.


July 2018

You and ME: An Update on Myalgic Encephalomyelitis for Psychologists by Rose Silvester

https://www.facebook.com/notes/nz-carers-of-kids-with-mecfsrelated-illnesses/you-and-me-an-update-on-myalgic-encephalomyelitis-for-psychologists-by-rose-silv/2102751053086637/ 

Calling it chronic fatigue is a bit like calling a pie “a crust”
Anna, age 16, personal communication, 2018.


Rose Silvester is a consultant clinical psychologist based in Wellington, New Zealand, currently working at the Regional Personality Disorder Service at Capital & Coast District Health Board (CCDHB). In the context of her son’s illness she has immersed herself in the literature available on ME/CFS and models of care for chronic illness. She is engaged with the global ME/CFS community of researchers, clinicians and advocates and has initiated a national carers support network (NZ carers of kids with ME/CFS and related illnessNZcare4ME) as well as a local carers support group.

This article was first published in the June 2018 edition of the Journal of the New Zealand College of Clinical Psychologists (NZCCP).


My son lives behind the closed door of a dark room. He has been there for two and a half years, he is 17, he has myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). I cannot unlock the door.

Unlike most other people who have this problem, his onset was not abrupt and not obviously triggered by an assault to the immune system, such as by one of the many associated viruses, or by vaccination, or any event that created significant stress for the body. Toward the end of his primary years, I found myself frequently making excuses for him, for why he was very bright but struggled to be on task, why he went from being in the top 10 in the school cross country to being hundreds of metres behind the last kid, why at soccer following the half time sugar hit that revved the other kids up, he was listless and just watched as the ball rolled past. I blamed it on the insomnia, night sweats, and headaches because they were certainly there, and I thought to myself “kids are weird—they grow out of it.”

And he did grow out of it—for a time. He had periods of many months where we thought the difficulties had stopped. By the time he reached high school, however, a small cold would see him confined to bed long after the cold symptoms had gone. There was nothing specifically wrong, no fever, vomiting, rash, or cough. He denied that he was tired or fatigued. Nothing. His batteries were just flat. These episodes began to get more frequent, more severe, and his recovery in between, less complete. During one memorable episode, I took him to the GP. He could hardly walk and had to lean against the wall of the corridor to make it to the office. He slurred his words, he was drowsy—he was clearly a very sick kid. After much shoulder shrugging and head scratching we were off for blood tests. While these revealed minor abnormalities (hypoglycaemia, slightly off thyroid function), a blood test could not possibly reveal the problem. These minor things, however, threw everyone off track. And there we remained for over a year. It was during this year that the door began to slowly close.

Most of the fourth term of year 10 at high school was spent at home. We tried to keep him going. He would get up, get ready for school, but be stopped in his tracks by body aches, headaches, and weakness. He was dizzy and fainted half a dozen times. His heart rate while standing would soar to 140 bpm and stay there. We know now that these early symptoms were the hallmark orthostatic symptoms of postural orthostatic tachycardia that often precede full syndrome ME/CFS. He spent most of the term at home and did gradually recover—enough to have a good summer. Again, we thought “it” whatever “it” was, was going to leave him alone. He was excited to go to school with his mates on the first day of year 11. At Wellington High School, year 11 kids are allowed to go to town at lunch time and he took full advantage of the freedom. He came home happy. That night, sometime while he slept, the door slammed shut. He has not been able to return to school.

Myalgic encephalomyelitis (my*al*gic + en*ceph*a*lo*my*eli*tis) (ME), is commonly referred to as chronic fatigue syndrome (ME/CFS). We eventually achieved this diagnosis, but too late to be aware of the cumulatively damaging effects of the episodes of unwellness that we now know were “crashes.” The need for careful pacing was never discussed. Too late too, to take advantage of the potential that managing his orthostatic symptoms more effectively may have reduced some of the stress his body was under.

The Institute of Medicine (IOM) describes ME/CFS is a serious, chronic disease that affects an estimated 0.5%–1% of people (Institute of Medicine, 2015). There is no known definitive aetiology or effective treatment. Diagnosing the disease remains a challenge, and patients often struggle with their illness for years before identification is made. Recovery of pre-illness functioning is rare. Seventy-five percent are unable to return to pre-illness levels of work or study. Many people with ME/CFS are more impaired in their functioning than those with other chronic and disabling illnesses, including type 2 diabetes mellitus, congestive heart failure, hypertension, depression, multiple sclerosis, and end-stage renal disease (Twisk, 2014). Women are more likely than men to be afflicted, and although peak onset is in adulthood, children also commonly get ME/CFS. It is estimated that as many as 90% of people (across all ranges of severity) are not diagnosed (Institute of Medicine 2015).

The cause remains unknown, but currently the most likely contender is that it is a systemic disease, and that in vulnerable (most likely genetically vulnerable) individuals, an assault to the immune system causes an abnormal immune response, which in turn causes an inflammatory reaction that affects the whole body right down to the level of mitochondrial energy production. In particular, it seems that the autonomic nervous system becomes unbalanced, leaving people stuck in a state of sympathetic overdrive—a constant state of fight or flight affecting heart rate and blood pressure (orthostatic regulation), temperature regulation, pupillary reaction, digestion, sensory filtering, emotional regulation, and so on. Pain in joints and/or the generalised ache of the first few days of the flu is usual. Cognitively, the effects can, for some, be devastating. Widespread endocrine abnormalities in many people suggest that the delicate balance of the hypothalamic-pituitary-adrenal axis has wobbled. Not surprisingly, sleep becomes inefficient and unrefreshing. Homeostasis is wrecked. It is exhausting. Post-exertional malaise is a hallmark symptom. It simply means that the window for tolerating any exertion, be it physical, cognitive, or emotional has narrowed. A marked worsening of symptoms occurs in the 12–72 hours following exertion. This worsening, sometimes called a crash, can persist for days, weeks, months, or years. Inter-episode recovery decreases with each crash. For around 25% of people, the window narrows to a point whereby activities of independent living are not possible. They are confined to their houses. Many are bed bound.

The pathophysiology of ME/CFS is very, very complicated. While recent research has identified a range of biomarkers and metabolic abnormalities in people with ME, these tests remain tools of research. Diagnosis is by symptom identification and exclusion of other illnesses that may present in a similar way. Over the last few decades, diagnostic criteria for ME/CFS have been widely debated. In 2015, the National Academy of Medicine published new diagnostic criteria for ME/CFS requiring the presence of: substantial impairment in activity that lasts 6 months or more and is accompanied by fatigue, post-exertional malaise, unrefreshing sleep, and either cognitive impairment or orthostatic intolerance (Institute of Medicine 2015). These criteria are, on the face of it, a massive simplification of a very complex picture in which the likelihood of multiple disease processes exists. Agreement and consistency of definition is, however, welcome.

The label “ME/CFS” has been similarly debated. Clinicians, researchers, and people with ME/CFS have pushed back, particularly against the label of chronic fatigue, arguing that it minimises the breadth and savagery of symptoms. It also has the unfortunate history of the misunderstanding and minimisation that came with derogatory labels such as “yuppie flu.” While the term CFS is rapidly on its way out, ME (for now) remains (grudgingly), and the IOM label of systemic exertional intolerance disease is on its way in (Institute of Medicine, 2015).

ME/CFS has not had an easy history, and it continues to sit uncomfortably. The diagnosis has fallen victim to the kind of stigma and marginalisation that is common when we are faced with things we cannot easily test or measure. The notion that ME/CFS can be formulated as a psychogenic disorder, such as conversion disorder or somatoform disorder has prevailed in both the medical and psychological communities.

Early hypotheses of psychological causation have long since been countered by growing research showing biological correlates of ME/CFS not found in depression or any other psychiatric disorder (Stein, 2005). The prevalence of known psychiatric disorders among patients with ME/CFS is similar to the rates in patients with other chronic, disabling medical conditions, such as rheumatoid arthritis; approximately 30%–40% (Thieme, Turk, & Flor, 2004). The World Health Organization classifies ME/CFS in the International Classification of Diseases, tenth revision as a neurological disorder (ICD 93.3). Little evidence exists for any disorder in this category conforming to a psychogenic formulation (Wilshire & Ward, 2016). Healthcare providers, however, remain sceptical about the physiological—rather than psychological—nature of the illness. “Once diagnosed, patients often complain of receiving hostility from their healthcare provider as well as being subjected to treatment strategies that exacerbate their symptoms” (Institute of Medicine, 2015). Within the ME/CFS community, anecdotes of gas- lighting and exclusion from treatment are the norm. I would suggest, where scepticism or doubt exists for health providers, that these notions are grossly outdated and perhaps “all in their heads.”

Psychology, and particularly cognitive behavioural therapy (CBT), has for some time been positioned in the centre of this discomfort. In recent decades, the officially recommended treatments for chronic fatigue syndrome (ME/CFS) have been graded exercise therapy (GET) and CBT. These treatments are formulated to satisfy the premise that ME/CFS symptoms are precipitated by factors such as trauma, prolonged stress, or personality factors, and are perpetuated by avoidance of activity and aberrant illness beliefs (Wilshire & Ward, 2016). The idea is that graded desensitisation (to the anxiety produced by activity) will help the individual to appreciate that pain and fatigue are not harmful. I recently Googled ME/CFS and CBT—the first entry that came up sums up this position:

…illness beliefs may lead to disability, as people obsess about their symptoms, entrench themselves in the conviction of organicity, and become disabled. Their marriages may break up; they may lose their jobs. The human consequences of these illness beliefs, in other words, may be considerable. Joining a sufferers’ support group that will irreversibly confer a label is really the last step on this pathway to disability. (Shorter, 2015)

Based on the assumption that psychological factors both precipitate and perpetuate the disorder, and in an attempt to provide evidence of the efficacy of CBT and GET, White and colleagues undertook a large-scale randomised trial (White, Goldsmith, Johnson, & Potts, 2011). This was colloquially referred to as the PACE trial. Reports published in reputable journals (including The Lancet) concluded that the PACE graded exercise and CBT protocols were moderately effective treatments for ME/CFS, leading to “recovery” in over one-fifth of patients. The trial’s size and subsequent promotion of CBT and GET as a gold standard treatment became hugely influential in the development of treatment guidelines, including the National Institute for Health and Care Excellence (NICE, 2007) and Centre for Disease Control (CDC) guidelines.

Soon after publication, however, there began a clamour of dissent. People with ME/CFS were perplexed, stating that the premise was incorrect and that, in their experience GET and CBT were not only ineffective, but were harmful. In forcing people with ME outside of their safe window of energy consumption, they risked a crash. The result, for many, was catastrophic. There also emerged significant concerns about the methodology of the trial. Sitting at the tip of this rather large iceberg of concerns was that the outcomes and analyses reported did not follow the original published protocol (Wilshire et al., 2018). This was troubling given that the purpose of a trial protocol is to prevent post hoc changes to methodology that may favour the study hypotheses. Also, it was doubtful whether the trial’s conclusions about treatment efficacy were justified by the evidence. David Tuller, a critic and prolific writer on the failures of the PACE trials reported a “bizarre paradox” (Tuller, 2015). The scores that determined whether someone qualified as disabled enough to enter the trial could simultaneously qualify them as “recovered” (by the definition of the outcome measures). A full 13% had “recovered” before the trial started, based on the change in protocol that occurred months after data collection ended (Tuller, 2015).

It is in this context that within a few years, the clamour turned into a furore, and accusations as strong as scientific fraud were levelled against the PACE trial authors by the ME/CFS research community. In 2015, an open letter was written to Richard Horton, Editor of The Lancet, by eminent researchers in the field of ME/CFS, including Ron Davis, Professor of Biochemistry and Genetics at Stanford University (and a current leading light in the ME/CFS research community as well as father to Witney, a young man with very severe ME/CFS). The letter raised concerns about “serious ethical breaches in the study” and stated that the flaws inherent in the study “have no place in published research.” This was strongly worded criticism, and went on to say the shortcomings were “of particular concern because of its significant impact on government policy, public health practice, clinical care, and decisions about disability insurance and other social benefits.” The Lancet was urged 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” (Davis et al., 2015).

While voluminous discussion and reanalysis has subsequently been published, reanalysis was hampered by the refusal of the original authors and PACE trial committee to release the original dataset for scrutiny. These data were, however, recently obtained as part of a Freedom of Information application, and made available to the public. In March this year, a new player walked onto this complex stage with the publication of a reanalysis of the PACE trial using this previously unavailable original data (Wilshire et al., 2018). Imagine my surprise when the author turned out to be Dr Carolyn Wilshire, from the School of Psychology at Victoria University. We talked about the big picture and her findings over coffee in Aro Street.

Carolyn Wilshire’s thorough and hopefully definitive reanalysis of the PACE trial concluded that, despite the power of the study afforded by the large sample size, the results were “modest, short- lived changes in self-report behaviour unaccompanied by objectively measurable changes.” She further commented that “it seems unlikely that further research based on these treatments will yield more favourable results” and “the time has come to look elsewhere for effective treatments” (Wilshire et al., 2018). Even the use of CBT for basic distress reduction has been called into question with the results of repeated patient surveys indicating that for many, CBT is harmful (Laws, 2017). Last year, in response to these contradictions, the CDC quietly changed its ME/CFS treatment guideline, removing any reference to GET and CBT, and clearly stating the likely harm (CDC, 2017). Similarly the NICE guidelines group announced a revision and specifically cited conflicts in the evidence for GET and CBT as a major basis for review (NICE, 2017). Current major National Institute of Health (the major US health research funder) research initiatives are focused on the pathophysiology of ME/CFS. The hope of the ME/CFS community is that these initiatives will play a key role in generating new treatment paradigms (Wilshire et al., 2018).

But the research initiatives to which Carolyn Wilshire refers are, in the scheme of things, in their infancy and comparatively poorly funded. Crowd funding and private donations for research remain common. For example, Ron Davis’ research has this year been funded by patients, and the Pineapple Fund, a fund provided by a private Bitcoin investor. Investigations into ME/CFS have lagged so far behind other disorders that some of the figures would be comical if they were not so tragic. Jorgen Jelstad (2016) quantified this inequity, and noted that although the measures of quality of life of people with ME fall below that of people with multiple sclerosis, more is spent on research into MS every year than has ever been spent on ME/CFS. Research into HIV/AIDS in the US attracts around 600 times the funding, although HIV affects similar numbers of people, with better outcomes. Male pattern baldness gets six times more federal funding than ME/CFS in the US (Jelstad, 2016). It is not so strange then, that it is taking time to find any credible answers to the ME/CFS enigma. Nancy Klimas, Professor of Microbiology and Immunology and one of the more prominent ME/CFS specialist clinicians (there are only a handful) was quoted in the New York times in 2009:

My HIV patients for the most part are hale and hearty thanks to three decades of intense and excellent research and billions of dollars invested. Many of my ME/CFS patients, on the other hand, are terribly ill and unable to work or participate in the care of their families. I split my clinical time between the two illnesses, and I can tell you if I had to choose between the two illnesses (in 2009) I would rather have HIV. (Klimas, 2009)

This lack of research is a barometer of a broader issue of the value that the health sector places on people with ME. Let me give you an example that is very close to home. A recent meeting for a very elderly relative who was moving to palliative care was attended by the geriatrician, rest home manager, charge nurse, dietician, social worker, and psychologist. While I am loath to sound petulant, my son, who is so very unwell, is seen by one physician around every 4 months. This physician has worked hard to consult and refer where possible. The waiting and time to get answers has however, been interminable. Even for some simple and commonly used specialist consultations it has been years. This is such a long time in a young person’s life at a critical developmental stage. Our health system is not designed to deal with complex problems involving multiple organ systems. If I had a magic wand I would conjure up specialist integrated teams of clinicians (physicians, cardiologists, endocrinologists, immunologists, neurologists, physiotherapists, occupational therapists, psychologists, and social workers) who would work together to optimise the management and quality of life for all people with ME.

So where does this leave psychology in supporting this population? Did you, like me, see the baby sailing through the air with the PACE trial bathwater? The downstream effect of the PACE study is that in all the fuss the real value of psychology for people with ME has been neglected and remains ambiguous. For myself, I know that there is a lot to be gained from acceptance of what-ifs of the past, the grief of the present, and the uncertainty of the future. De-fusing from the guilt and fear demons that come flapping in the night. It has become important to be mindful of the moment and to connect with what is present, here and now, in all its limitations as well as possibilities—and to find value in this. And…to remain open to a new identity as it emerges: advocate, activist, educator, supporter, and friend to the community of people with ME and their carers. The support my son needs, if he were well enough, would be very similar and would also include finding the window of energy tolerance, establishing a routine around this and developing values and an identity within his limitations. You may notice that none of this involves an assumption that if he just pushed a little harder he would be ok, or a focus on aberrant illness beliefs. We went there. It failed.

Late last year the face of ME/CFS changed. Completely. Unrest, a documentary by Jennifer Brea was released and subsequently avalanched with awards. Jenn (yeah it feels like she’s been in my living room), a person with ME wrote and directed Unrest, largely from her bed. It is brave, informative and heart-breaking. She collaborated with families, researchers and clinicians— including Ron Davis and his family—and provided a focus for people with ME and their advocates around the world. Unrest has been shown at thousands of public education events and is now being used as part of the curriculum at universities such as Harvard Medical School. From the momentum that Unrest unleashed, MEAction was born. This group works tirelessly to promote Unrest and to galvanise a community of activists. A clear direction for advocacy and education has now been illuminated. Please watch Unrest. It is on Netflix and Itunes.

So…what of my son? I wrote a paragraph on how he is now, then decided that he would not want you to know the details. He remains severely disabled. The door to the room that confines him is firmly shut and has a thousand locks on it. In our hands there are a thousand keys. Every 4 months or so, when we meet with his very caring physician, we get to choose whether we keep wriggling the current key in the current lock, or try a different combination. In the vacuum of knowledge about the real mechanisms that drive ME/CFS there is little to guide our choice. And so, we wait.

Thanks to my friends (NZcare4ME) who are along for the ride, and helped with references.

References

Center for Disease Control. (2017). Myalgic encephalomyelitis/chronic fatigue syndrome. Retrieved from https://www.cdc.gov/me-cfs/index.html

Davis, R., Jonathan, C. W., Jason, L., Levin, B., Racaniello, V. R., & Reingold, A. (2015). An open letter to Dr Richard Horton and The Lancet. Virology Blog. Retrieved from http://www.virology.ws/2015/11/13/an- open-letter-to-dr-richard-horton-and-the-lancet/

Institute of Medicine. (2015) Beyond myalgic encephalomyelitis/chronic fatigue syndrome: Redefining an illness. Washington, DC: The National Academies Press.

Jelstad, J. (2016). The male pattern baldness disease? Chronic fatigue syndrome’s chronic lack of research funding. Retrieved from https://www.healthrising.org/blog/2016/05/04/chronic-lack-funds-chronic-fatigue- syndrome-mecfs-research/

Klimas, N. (2009). A virus linked to chronic fatigue syndrome. New York Times Laws, K. R. (2017). Distress signals: Does cognitive behavioural therapy reduce or increase distress in chronic fatigue syndrome/myalgic encephalomyelitis? Journal of Health Psychology, 22(9), 1177–1180. National Institute for Health and Clinical Excellence. (2007). Chronic fatigue syndrome/myalgic encephalomyelitis (or encephalopathy): Diagnosis and management of CFS/ME in adults and children. Retrieved from https://www.nice.org.uk/guidance/cg53/evidence/full-guideline-pdf-196524109

National Institute for Health and Clinical Excellence. (2017). Surveillance report. Chronic fatigue syndrome/myalgic encephalomyelitis (or encephalopathy): diagnosis and management (2007) NICE guideline CG53. Retrieved from https://www.nice.org.uk/guidance/cg53/resources/surveillance-report-2017-chronic-%20fatigue-syndromemyalgic-encephalomyelitis-or-encephalopathy-diagnosis-and-management-2007-nice-%20guideline-cg53-4602203537/chapter/how-we-made-the-decision#how-we-made-the-decision

Shorter, E. (2015) Chronic fatigue in the context of the history of medicine. Retrieved from https://www.psychologytoday.com/us/blog/how-everyone-became-depressed/201502/chronic-fatigue-%20in-the-context-the-history-medicine

Stein, E. (2005). Chronic fatigue syndrome. Psychiatric Treatment Guidelines. Retrieved from https://anzmes.org.nz/

Thieme, K., Turk, D. C., & Flor, H. (2004). Comorbid depression and anxiety in fibromyalgia syndrome: relationship to somatic and psychosocial variables. Psychosomatic Medicine, 66, 837–844.

Tuller, D. (2015). Trial by error: The troubling case of the PACE chronic fatigue syndrome study. Retrieved from http://www.virology.ws/2015/10/22/trial-by-error-ii/

White, P. D., Goldsmith, K. A., Johnson, A. L., & Potts, L. (2011). Comparison of adaptive pacing therapy, cognitive behaviour therapy, graded exercise therapy, and specialist medical care for chronic fatigue syndrome (PACE): a randomised trial. The Lancet. 377(9768), 823–36.

Wilshire, C. R., Kindlon, T., Courtney, R., Matthees, A., Tuller, D., Geraghty, K., & Levin, B. (2018). Re-thinking the treatment of chronic fatigue syndrome—a reanalysis and evaluation of findings from a recent major trial of graded exercise and CBT. BMC, 6, 6. Retrieved from https://bmcpsychology.biomedcentral.com/articles/10.1186/s40359-018-0218-3#Bib1

Wilshire, C. E., & Ward, T. (2016). Psychogenic explanations of physical illness: time to examine the evidence. Perspectives on Psychological Science, 11(5), 606.


June 2018

Trial By Error: An Open Letter to The Lancet, Two Years On

http://www.virology.ws/2018/06/19/trial-by-error-an-open-letter-to-the-lancet-two-years-on/

19 June 2018

By David Tuller, DrPH

This morning, Professor Racaniello sent the following e-mail to Richard Horton, editor of The Lancet. The subject heading: “Another open letter about the PACE trial.” He cc’d the three lead PACE investigators and the public relations office at Queen Mary University of London. Virology Blog’s previous open letter to The Lancet about the PACE trial was sent and posted in February, 2016.

**********

Dear Dr. Horton:

In February, 2011, The Lancet published an article called “Comparison of adaptive pacing therapy, cognitive behaviour therapy, graded exercise therapy, and specialist medical care for chronic fatigue syndrome (PACE): a randomized trial.” [1] The article reported that two rehabilitative approaches, cognitive behavioural therapy (CBT) and graded exercise therapy (GET), were effective and safe treatments for chronic fatigue syndrome, also often referred to as myalgic encephalomyelitis, ME/CFS and CFS/ME. The PACE study received international attention and has had widespread influence on research, treatments prescribed for patients, and attitudes toward the illness of both the medical community and the public at large.

At the press conference promoting the Lancet paper, one of the lead investigators stated that twice as many participants in the treatment groups got “back to normal,” compared to those in the other study arms. [2] An accompanying Lancet commentary similarly claimed that these “back-to-normal” participants had met a “strict criterion for recovery.” [3]

In fact, we now know that 13 % of the participants qualified at baseline as “recovered” or “within the normal range” for one of the study’s two primary measures, self-reported physical function–even as they were simultaneously classified as disabled enough on the same measure to enter the study. [4] This anomaly, which occurred because the investigators weakened key outcome thresholds after data collection, invalidates any claims that patients “recovered” or got “back to normal.” The overlap in entry and outcome criteria is only one of the trial’s unacceptable methodological lapses.

The treatments investigated in the PACE trial were based on the hypothesis that ME/CFS patients harbor “unhelpful” convictions about having an ongoing organic disease and that the perpetuation of their devastating symptoms is the result of deconditioning. In contrast, a 2015 review from the U.S. Institute of Medicine (now the National Academy of Medicine), reported that ME/CFS is a complex, multi-system illness characterized by neurological, immunological, autonomic, and energy metabolism dysfunctions. [5] The cardinal symptom, noted the review, is a systemic intolerance to exertion; if patients exceed their available energy resources, they can suffer serious and prolonged relapses.

After The Lancet published the first PACE results, ME/CFS patients and advocates immediately pointed out major flaws. But few people outside the field took notice until the science site Virology Blog published a 15,000-word investigation by David Tuller, a public health researcher and journalist at the University of California, Berkeley, in October of 2015. [6] Subsequently, in February of 2016, many of us signed an open letter to The Lancet requesting an independent investigation of the study. [7]

Since then, much has happened:

* In August of 2016, a U.K. tribunal, citing that open letter, ordered Queen Mary University of London to release raw trial data from the PACE study, sought by Australian patient Alem Matthees in a freedom of information request so that he and others could calculate the outcomes promised in the PACE trial protocol. [8]

* Analyses of these data [9], including a study published in BMC Psychology in March [10], have confirmed what has long been argued: The PACE investigators engaged in such extensive outcome-switching that they were able to report dramatically better findings than the null or minimal results obtained under the original measures they promised in their protocol.

* The U.S. Agency for Healthcare Research and Quality (AHRQ) downgraded its recommendations for CBT and GET. [11] This downgrading occurred after the agency removed from its analysis the PACE trial and other studies using overly broad selection criteria that generated cohorts of patients with a grab-bag of fatiguing conditions. And while the PACE trial claimed that GET is safe, AHRQ found that the therapy was associated with more adverse events.

* Last summer, the U.S. Centers for Disease Control abandoned the recommendations that ME/CFS patients be treated with CBT and GET [12], having already removed references to the PACE trial. A couple of months later, the U.K. National Institute for Health and Care Excellence announced that it would pursue a full update of its 2007 guidance, citing concerns about the reliability and validity of the evidence base. [13]

* Earlier this year, a report from the Dutch Health Council recommended that GET should not be used in the Netherlands as a treatment for the illness. [14]

* In March, a group of leading American clinicians who specialize in ME/CFS unanimously agreed that the two PACE treatments are inappropriate and possibly harmful for patients with the illness and should therefore not be prescribed. [15]

Given the worldwide impact of PACE, we urge The Lancet to do what the open letter two years ago requested: commission an independent re-analysis of the individual-level 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 domains of psychiatry and psychological medicine and predominantly from outside the U.K. They should also be completely independent of, and have no conflicts of interests involving, the PACE investigators and the funders of the trial.

Thank you for your quick attention to this matter.

Sincerely,

Dharam V. Ablashi, DVM, MS, Dip Bact
Scientific Director, HHV-6 Foundation
Santa Barbara, California, USA
Former Senior Investigator
National Cancer Institute
National Institutes of Health
Bethesda, Maryland, USA

Michael Allen, PhD
Clinical Psychologist (retired)
San Francisco, California, USA

Christopher Armstrong, PhD
Bio21 Molecular Science & Biotechnology Institute
Department of Biochemistry and Molecular Biology
University of Melbourne
Melbourne, Victoria, Australia

James N. Baraniuk, MD
Professor of Medicine
Georgetown University
Washington, DC, USA

Lisa F. Barcellos, PhD
Professor of Epidemiology
School of Public Health
California Institute for Quantitative Biosciences
University of California, Berkeley
Berkeley, California, USA

Lucinda Bateman, MD
Medical Director
Bateman Horne Center
Salt Lake City, Utah, USA

Molly Brown, PhD
Assistant Professor
Department of Psychology
DePaul University
Chicago, Illinois, USA

Robin Callender Smith, PhD
Professor of Media Law
Centre for Commercial Law Studies
Queen Mary University of London
Barrister and Information Rights Judge
London, England, UK

John Chia, MD
Clinician and Researcher
EV Med Research
Lomita, California, USA

Lily Chu, MD, MSHS
Independent Researcher
Burlingame, California, USA

Joan Crawford, CPsychol, CEng, CSci, MA, MSc
Chartered Counselling Psychologist
Chronic Pain Management Service
St Helens Hospital
St Helens, England, UK

Janet L Dafoe, PhD
Child Psychologist in Private Practice
Palo Alto, California, USA

Todd E. Davenport, PT, DPT, MPH, OCS
Professor & Program Director
Department of Physical Therapy
Thomas J. Long School of Pharmacy & Health Sciences
University of the Pacific
Stockton, California, USA
Workwell Foundation
Ripon, California, USA

Ronald W. Davis, PhD
Professor of Biochemistry and Genetics
Stanford University
Stanford, California, USA

Lucy Dechene, PhD
Professor of Mathematics (retired)
Fitchburg State University
Fitchburg, Massachusetts, USA

Simon Duffy, PhD, FRSA
Director
Centre for Welfare Reform
Sheffield, England, UK

Jonathan C.W. Edwards, MD
Emeritus Professor of Medicine
University College London
London, England, UK

Valerie Eliot Smith
Barrister and Visiting Scholar
Centre for Commercial Law Studies
Queen Mary University of London
London, England, UK

Derek Enlander, MD
Clinician in Private practice
New York, New York, USA

Meredyth Evans, PhD
Clinical Psychologist and Researcher
Chicago, Illinois, USA

Kenneth J. Friedman, PhD
Associate Professor of Physiology and Pharmacology (retired)
New Jersey Medical School
University of Medicine and Dentistry of New Jersey
Newark, New Jersey, USA

Robert F. Garry, PhD
Professor of Microbiology and Immunology
Tulane University School of Medicine
New Orleans, Louisiana, USA

Keith Geraghty, MPH, PhD
Honorary Research Fellow
Division of Population Health, Health Services Research & Primary Care
School of Health Sciences
University of Manchester
Manchester, England, UK

Simin Ghatineh, MSc, PhD
Biochemist
London, England, UK

Ian Gibson, PhD
Former Member of Parliament for Norwich North
Former Dean, School of Biological Sciences
University of East Anglia
Honorary Senior Lecturer and Associate Tutor
Norwich Medical School
University of East Anglia
Norwich, England, UK

Mike Godwin, JD
Attorney and Author
Distinguished Senior Fellow
R Street Institute
Washington, DC, USA

Rebecca Goldin, PhD
Professor of Mathematics
George Mason University
Fairfax, Virginia, USA

Alan Gurwitt, MD
Clinician in Private Practice (retired)
Associate Clinical Professor, Yale Child Study Center (retired)
New Haven, Connecticut, USA
Associate Clinical Professor, University of Connecticut Dept of Psychiatry (retired)
Storrs, Connecticut, USA
Lecturer, Harvard Medical School (retired)
Boston, Massachusetts, USA

Geoffrey Hallmann, LLB, DipLegPrac
Former Lawyer (Disability and Compensation)
Lismore, New South Wales, Australia

Maureen Hanson, PhD
Liberty Hyde Bailey Professor
Department of Molecular Biology and Genetics
Cornell University
Ithaca, New York, USA

Malcolm Hooper, PhD, BPharm, MRIC, CChem
Emeritus Professor of Medicinal Chemistry
University of Sunderland
Tyne and Wear, England, UK

Leonard A. Jason, PhD
Professor of Psychology
DePaul University
Chicago, Illinois, USA

Michael W. Kahn, MD
Assistant Professor of Psychiatry
Harvard Medical School
Boston, Massachusetts, USA

Jon D. Kaiser, MD
Clinical Faculty
Department of Medicine
University of California, San Francisco
San Francisco, California, USA

David L. Kaufman, MD
Center for Complex Diseases
Mountain View, California
Member, The ME/CFS Collaborative Research Center at Stanford
Palo Alto, California, USA

Betsy Keller, PhD, FACSM
Professor, Department of Exercise & Sport Sciences
Ithaca College
Ithaca, New York, USA

Nancy Klimas MD
Director, Institute for Neuro-Immune Medicine
Nova Southeastern University
Director, Miami VA Medical Center GWI and CFS/ME Program
Miami, Florida, USA

Andreas M. Kogelnik, MD, PhD
Director
Open Medicine Institute
Mountain View, California, USA

Richard Kwiatek, MBBS, FRACP
Rheumatologist and Independent Researcher
Northern Adelaide Local Health Network
Adelaide, South Australia, Australia

Eliana M. Lacerda, MD, MSc, PhD
Clinical Assistant Professor
International Centre for Evidence in Disability
Faculty of Infectious and Tropical Diseases
London School of Hygiene & Tropical Medicine
London, England, UK

Charles W. Lapp, MD
Medical Director
Hunter-Hopkins Center
Charlotte, North Carolina, USA

Bruce Levin, PhD
Professor of Biostatistics
Columbia University
New York, New York, USA

Donald Lewis, MBBS, FRACGP, DRACOG
Medical Director
CFS Discovery
Melbourne, Victoria, Australia

Alan R. Light, PhD
Professor of Anesthesiology
Professor of Neurobiology and Anatomy
University of Utah
Salt Lake City, Utah, USA

Vincent C. Lombardi, PhD
Director of Research
Nevada Center for Biomedical Research
Reno, Nevada, USA

Alex Lubet, PhD
Professor of Music
Head, Interdisciplinary Graduate Group in Disability Studies
Affiliate Faculty, Center for Bioethics
Affiliate Faculty, Center for Cognitive Sciences
University of Minnesota
Minneapolis, Minnesota, USA

Steven Lubet, JD
Williams Memorial Professor of Law
Northwestern University Pritzker School of Law
Chicago, Illinois, USA

David F. Marks, PhD
Editor
Journal of Health Psychology
& Health Psychology Open
London, England, UK

Sonya Marshall-Gradisnik, PhD
Professor of Immunology
Co-Director, National Centre for Neuroimmunology and Emerging Diseases
Griffith University
Gold Coast, Queensland, Australia

Marlon Maus, MD, DrPH, FACS
DrPH Program Director
School of Public Health
University of California, Berkeley
Berkeley, California, USA

Neil R McGregor. BDS, MDSc, PhD
Clinical Associate Professor
Faculty of Medicine, Dentistry and Health Sciences
Bio21 Molecular Science & Biotechnology Institute
University of Melbourne.
Melbourne, Victoria, Australia

Patrick E. McKnight, PhD
Professor of Psychology
George Mason University
Fairfax, Virginia, USA

Marvin S. Medow, PhD
Professor of Pediatrics and Physiology
Chairman, New York Medical College IRB
Associate Director of The Center for Hypotension
New York Medical College
Hawthorne, New York, USA

Jose G. Montoya, MD, FACP, FIDSA
Professor of Medicine
Division of Infectious Diseases and Geographic Medicine
Stanford University School of Medicine
Stanford, California, USA
Director, Palo Alto Medical Foundation Toxoplasma Serology Laboratory
National Reference Center for the Study and Diagnosisof Toxoplasmosis
Palo Alto, California, USA

Sarah Myhill, MBBS
Clinician in Private Practice
Knighton, Wales, UK

Luis Nacul, MD, PhD
Clinical Associate Professor
International Centre for Evidence in Disability
Faculty of Infectious and Tropical Diseases
London School of Hygiene & Tropical Medicine
London, England, UK

Heidi Nicholl, PhD
Chief Executive Officer
Emerge Australia
Melbourne, Victoria, Australia

James M. Oleske, MD, MPH
François-Xavier Bagnoud Professor of Pediatrics
Senator of RBHS Research Centers, Bureaus, and Institutes
Director of Division of Pediatrics Allergy, Immunology & Infectious Diseases
Department of Pediatrics
Rutgers New Jersey Medical School
Newark, New Jersey, USA

Elisa Oltra, PhD
Professor of Molecular and Cellular Biology
Catholic University of Valencia School of Medicine
Valencia, Spain

Nigel Paneth, MD, MPH
University Distinguished Professor
Depts of Epidemiology & Biostatistics and Pediatrics & Human Development
College of Human Medicine
Michigan State University
East Lansing, Michigan, USA

Richard Podell, MD, MPH
Clinical Professor, Department of Family Medicine
Rutgers-Robert Wood Johnson Medical School
New Brunswick, New Jersey, USA

Nicole Porter, PhD
Psychologist in Private Practice
Rolling Ground, Wisconsin, USA

Vincent R. Racaniello, PhD
Professor of Microbiology and Immunology
Columbia University
New York, New York, USA

Arthur L. Reingold, MD
Professor of Epidemiology
University of California, Berkeley
Berkeley, California, USA

Peter C. Rowe, MD
Professor of Pediatrics
Johns Hopkins University School of Medicine
Baltimore, Maryland, USA

Michael Scott, PhD
Clinician/Researcher
Psychological Therapies Unit
Liverpool, England, UK

Charles Shepherd, MB BS
Honorary Medical Adviser to the ME Association
Buckingham, England, UK

Christopher R. Snell, PhD
Scientific Director
WorkWell Foundation
Ripon, California, USA

Nigel Speight, MA, MB, BChir, FRCP, FRCPCH, DCH
Pediatrician
Durham, England, UK

Donald R. Staines, MBBS, MPH, FAFPHM, FAFOEM
Clinical Professor
Menzies Health Institute Queensland
Co-Director
National Centre for Neuroimmunology and Emerging Diseases
Griffith University
Gold Coast, Queensland, Australia

Philip B. Stark, PhD
Professor of Statistics
University of California, Berkeley
Berkeley, California, USA

Eleanor Stein, MD, FRCP(C)
Psychiatrist in Private Practice
Assistant Clinical Professor
University of Calgary
Calgary, Alberta, Canada

Staci Stevens, MA
Founder, Exercise Physiologist
Workwell Foundation
Ripon, California, USA

Julian Stewart, MD, PhD
Professor of Pediatrics, Physiology and Medicine
Associate Chairman for Patient Oriented Research
Director, Center for Hypotension
New York Medical College
Hawthorne, New York, USA

Leonie Sugarman, PhD
Emeritus Associate Professor of Applied Psychology
University of Cumbria
Carlisle, England, UK

John Swartzberg, MD
Clinical Professor Emeritus
School of Public Health
University of California, Berkeley
Berkeley, California, USA

Ronald G. Tompkins, MD, ScD
Summer M Redstone Professor of Surgery
Harvard Medical School
Boston, Massachusetts, USA

Barbara True, MD, FRACP
Private Practice
Wakefield Rheumatology
Adelaide, South Australia, Australia

Samuel Tucker, MD
Former Assistant Clinical Professor of Psychiatry
University of California, San Francisco
San Francisco, California, USA

David Tuller, DrPH
Lecturer in Public Health and Journalism
University of California, Berkeley
Berkeley, California, USA

Rosemary A. Underhill, MBBS, MRCOG, FRCSE
Physician, Independent Researcher
Palm Coast, Florida, USA

Derya Unutmaz, MD
Professor
The Jackson Laboratory for Genomic Medicine
Farmington, Connecticut, USA

AM Uyttersprot, MD
Neuropsychiatrist
AZ Jan Portaels
Vilvoorde, Belgium

Rosamund Vallings, MNZM, MBBS
General Practitioner
Auckland, New Zealand

Linda van Campen, MD
Cardiologist
Stichting Cardiozorg
Hoofddorp, The Netherlands

Mark VanNess, PhD
Professor of Health, Exercise & Sports Sciences
University of the Pacific
Stockton, California, USA
Workwell Foundation
Ripon, California, USA

Mark Vink, MD
Family Physician
Soerabaja Research Center
Amsterdam, The Netherlands

Frans Visser, MD
Cardiologist
Stichting Cardiozorg
Hoofddorp, The Netherlands

Tony Ward, MA (Hons), PhD, DipClinPsyc
Registered Clinical Psychologist
Professor of Clinical Psychology
School of Psychology
Victoria University of Wellington
Wellington, New Zealand
Adjunct Professor, School of Psychology
University of Birmingham
Birmingham, England, UK
Adjunct Professor, School of Psychology
University of Kent
Canterbury, England, UK

William Weir, FRCP
Infectious Disease Consultant
London, England, UK

John Whiting, MD
Specialist Physician in Private Practice
Brisbane, Queensland, Australia

Sadie Whittaker, PhD
Chief Scientific Officer
Solve ME/CFS Initiative
Los Angeles, California, USA

Carolyn Wilshire, PhD
Senior Lecturer
School of Psychology
Victoria University of Wellington
Wellington, New Zealand

Marcie Zinn, PhD
Cognitive Neuroscience and Data Science
Center for Community Research
DePaul University
Chicago, Illinois, USA
Associate Editor, BMC Journal of Translational Medicine

___________

[1] White PD et al. 2011. Comparison of adaptive pacing therapy, cognitive behaviour therapy, graded exercise therapy, and specialist medical care for chronic fatigue syndrome (PACE): a randomised trial. The Lancet, 377: 823–836

[2] Boseley S. 2011. Study finds therapy and exercise best for ME. The Guardian, 18 Feb. Available at: https://www.theguardian.com/society/2011/feb/18/study-exercise-therapy-me-treatment (accessed on April 23, 2018)

[3] Bleijenberg G, Knoop H. 2011. Chronic fatigue syndrome: where to PACE from here? The Lancet, 377: 786-788

[4] Wilshire C et al. 2016. Can patients with chronic fatigue syndrome really recover after graded exercise or cognitive behavioural therapy? A critical commentary and preliminary re-analysis of the PACE trial. Fatigue: Biomedicine, Health & Behavior, 14 Dec. Available at: http://www.tandfonline.com/doi/full/10.1080/21641846.2017.1259724 (accessed on April 23, 2018)

[5] U.S. Institute of Medicine (now National Academy of Medicine). 2015. Beyond myalgic encephalomyelitis/chronic fatigue syndrome: redefining an illness. The National Academies: Washington, DC, USA.

[6] Tuller D. 2015. Trial by error: the troubling case of the PACE chronic fatigue syndrome trial. VirologyBlog, 21-23 Oct. Available at: http://www.virology.ws/2015/10/21/trial-by-error-i/ (accessed on April 23, 2018)

[7] Racaniello V. 2016. An open letter to The Lancet, again. VirologyBlog, 10 Feb. Available at: http://www.virology.ws/2016/02/10/open-letter-lancet-again/ (accessed on April 23, 2018)

[8] Rehmeyer J. 2016. Bad science misled millions with chronic fatigue syndrome. Here’s how we fought back. STAT, 21 Sept. Available at: https://www.statnews.com/2016/09/21/chronic-fatigue-syndrome-pace-trial/ (accessed on April 23, 2018)

[9] Geraghty K. 2017. ‘PACE-Gate’: when clinical trial evidence meets open data access. Journal of Health Psychology, 22: 1106-1112

[10] Wilshire C et al. 2018. Rethinking the treatment of chronic fatigue syndrome—a reanalysis and evaluation of findings from a recent major trial of graded exercise and CBT. BMC Psychology; published online 22 March. Available at: https://bmcpsychology.biomedcentral.com/articles/10.1186/s40359-018-0218-3 (accessed on April 23, 2018)

[11] Smith M et al. 2016. Diagnosis and treatment of myalgic encephalomyelitis/chronic fatigue syndrome; addendum. U.S. Agency for Healthcare Research and Quality. July. Available at: https://www.ncbi.nlm.nih.gov/books/NBK379582/ (accessed on April 23, 2018)

[12] Rehmeyer J, Tuller D. 2017. Why did it take the CDC so long to reverse course on debunked treatments for chronic fatigue syndrome? STAT, 25 Sept. Available at: https://www.statnews.com/2017/09/25/chronic-fatigue-syndrome-cdc/ (accessed on April 23, 2018)

[13] Whipple T. 2017. Mutiny by ME sufferers forces a climbdown on exercise treatment. The Times, 25 Sept.

[14] Health Council of the Netherlands. 2018. More scientific research on ME/CFS is needed to serve patients better. 19 March. Available at: https://www.gezondheidsraad.nl/en/news/more-scientific-research-on-mecfs-is-needed-to-serve-patients-better (accessed on April 23, 2018)

[15] Tucker M. 2018. Much can be done to ease ‘chronic fatigue syndrome’ symptoms. Medscape, 12 March. Available at: https://www.medscape.com/viewarticle/893766 (accessed on April 23, 2018)

(Many thanks to Mary Dimmock for helping to contact the signatories.)


June 2018

ME Association: The 2018 Invest in ME Research Conference Report – Dr Charles Shepherd

http://www.meassociation.org.uk/2018/06/the-2018-invest-in-me-research-conference-report-dr-charles-shepherd-14-june-2018/

The 2018 Invest in ME Research Conference Report – Dr Charles Shepherd | 14 June 2018

Dr Charles Shepherd provides a summary report of the 13th Invest in ME Research Conference that took place in London on 1st June – http://www.meassociation.org.uk/wp-content/uploads/Dr-Shepherd-IiMER-Conference-Report-2018-13.06.18.pdf

“The conference again took place at One Great George Street – an impressive Edwardian building, with equally impressive conference facilities, that sits opposite St James’s Park in London.

“As usual, the audience consisted of people with ME/CFS, carers, charity representatives, health professionals and researchers, from the UK and overseas. The conference was chaired by Dr Ian Gibson with his usual wit and enthusiasm.

“Overall, this was an interesting and enjoyable meeting that covered a number of important overseas research initiatives, as well as some clinical presentations that are more relevant to the here and now situation facing people with ME/CFS.

“Thank you to everyone who was involved in the organisation of the conference.”

To read and download Dr Shepherd’s report –

http://www.meassociation.org.uk/wp-content/uploads/Dr-Shepherd-IiMER-Conference-Report-2018-13.06.18.pdf

To order the DVDs from Invest in ME of all the conference talks, go to –

http://www.investinme.eu/IIMEC13-DVD-Order.shtml


June 2018

What Doctors Don’t Tell You: ME: the cure that went away

https://www.wddty.com/magazine/2018/june/me-the-cure-that-went-away.html

Bryan Hubbard

June 2018

Chronic fatigue and ME could be dramatically improved with exercise and therapy, a landmark study discovered. But it was bad science, and the cure was never there.

Controversy has always dogged chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME), the mysterious condition that leaves a patient tired all the time and exhausted from the slightest exertion. The minority of doctors who even believed their patient had an actual physical problem—as opposed to the rest who suspected it was more to do with mind than matter—were perplexed. Then, seven years ago, medicine thought they’d finally figured out how to treat it: patients could get better by combining exercise and cognitive behavioral therapy (CBT), the ‘talking cure.’

It was as if a light had been switched on in a darkened room, and it all came from one 2011 study, called the PACE trial, which concluded that the two approaches dramatically improved the sufferers’ fatigue—and around 22 percent went on to achieve a full recovery, the researchers claimed in a press conference. 1

But it’s all unraveling. Another research team has looked at the raw data that underpinned the PACE study and found that the therapies had “no long-term benefits at all.” The 60 percent improvement reported by the PACE researchers was reduced to just 20 percent in the reanalysis, and the 22 percent who had experienced a full recovery evaporated to just 8 percent. 2

To make matters worse, the data had to be crow-barred from the PACE research team. Freedom of information requests had been ignored, and it took two tribunals to get the researchers—who had recruited a $285,000 legal team to defend them—to conform with the request.

In a separate move, WDDTY columnist Dr Sarah Myhill is calling on the General Medical Council (GMC), which regulates the conduct of doctors in the UK, to mount an investigation. She is accusing the PACE researchers of scientific fraud and breaching ‘good medical practice.’

Out-paced

Looking at the raw data of the PACE study, researchers from the University of Wellington in New Zealand discovered that almost all the benefits of graded exercise—where the intensity and duration of activity slowly increase—and CBT disappear when the definition of ‘patient recovery’ is adhered to throughout the duration of the trial and when assessing patients’ outcomes afterwards.

The PACE researchers established what they meant by patient ‘improvement’ and ‘recovery’—which included established thresholds that were statistically measurable—before the study began. However, once the study was underway, they weakened their own protocols dramatically, and a patient would be considered to have ‘recovered’ even when their symptoms had worsened during the trial. The bar for good physical function was lowered so far that even an 80-year-old would have passed, other researchers noted.

Ultimately, the assessment of whether a participant had recovered was determined entirely by the patient—and this was after they had been shown glowing testimonials about the therapies they were getting halfway through the study.

When the original protocols for recovery were reapplied—along with other everyday measures such as returning to work—all the benefits announced by the PACE researchers disappeared. Rates of recovery were “consistently low,” the researchers said, and were hardly better than those being achieved by standard treatment. As lead researcher Carolyn Wilshere put it, the PACE researchers had “moved the goalposts.”

Legal pace

In Dr Myhill’s call to the GMC to investigate the PACE researchers, she is claiming that they have committed ‘scientific fraud.’ In a letter to Sir Terence Stephenson, GMC chairman, she cites three definitions laid out by the UK Fraud Act of 2006—fraud by false representation, fraud by failing to disclose information and fraud by abuse of position—which she wants the GMC to investigate.

She also argues that CFS/ME patients have been harmed by the therapies promoted by the PACE researchers, and she is urging them to also write to the GMC. “The PACE trial has effectively determined CFS/ME as a psychological condition. As a result, patients who suffer what is, in fact, a serious and debilitating physical condition have been subject to therapies which at best are ineffective and at worse exacerbate the condition,” she writes.

Keeping pace

Within months of the PACE results being published, doctors had quickly embraced the dual approach. In the UK, the National Institute for Health and Care Excellence (NICE) established it as the standard treatment, and, more bizarrely, the government’s Department for Work and Pensions (DWP) was also recommending it. But the DWP wasn’t an innocent bystander: it was shelling out millions in benefits to the country’s 250,000 ME sufferers, and it also happened to have funded the PACE trial to the tune of about $7 million. In the US, the Centers for Disease Control and Prevention (CDC), which had worked closely with two of the PACE researchers, Peter White from Queen Mary University in London and Michael Sharpe from Oxford University, also recommended the therapy as the way forward.

The PACE results had pleased both camps in medicine: those that believed that ME was ‘all in the head’ and others who suspected there had to be a viral cause. The PACE researchers were acolytes of psychiatrist Simon Wessely at King’s College London, who squared the circle with his hypothesis that a virus or some organic trigger may have kick-started the problem, but it was prolonged by the morbid thoughts of the sufferer. “The symptoms and disability of CFS are perpetuated predominantly by dysfunctional illness beliefs and coping behaviors,” he said. 3

While doctors celebrated, the analysis just wasn’t ringing true for many sufferers, who couldn’t believe that either approach was of much use. In fact, whenever they exercised, they collapsed with exhaustion immediately afterward, and were often confined to bed, as ME sufferer Sally Burch related after she had been advised by her doctor to take three brisk walks a day. “Those short walks were causing me to get out of breath, and to feel light-headed and dizzy. As the days went by, I found I was able to walk shorter and shorter distances before I ended up in a heap on the ground, trying to make the world stay still. Something was very wrong.” 4

Pace of change

Other sufferers thought there was something very wrong with the findings of the PACE trial, too. CFS sufferer Alem Matthees in Australia put in the first freedom of information request to see the underlying data, and he was soon joined by six scientists from Stanford University, who demanded a full independent investigation.

Even though the raw data was being kept under wraps, other researchers were able to spot anomalies. David Tuller at the University of California, Berkeley, discovered that 13 percent of the 641 CFS/ME sufferers recruited into the original trial had ‘recovered’ even before the trial had started, at least according to the very loose definition of ‘recovery’ the researchers were using.

Stung by the mounting criticism, the PACE researchers claimed that their critics were “young men, borderline sociopaths or psychopathic”—hardly a fitting description of scientists from Stanford University—before claiming they had been threatened and harassed, which was later found to be untrue.

Finally, they issued a new analysis of their original data, in which they concluded that the participants who hadn’t improved were simply afraid of exercise. 5

All of this puts our understanding about CFS/ME—what it is, what causes it and how it can be treated—back to square one. It’s clearly not ‘all in the mind’—or ‘yuppie flu,’ as it was once disparagingly described—and this acceptance is at least allowing new theories about what it might be to flourish.

References

1              Lancet, 2011; 377: 823-36

2              BMC Psychol, 2018; 6: 6

3              Gen Hosp Psychiatry, 1997; 19: 185-99

4              www.sallyjustme.blogspot.co.uk

5              Lancet Psychiatry, 2015; 2: 141-52


May 2018

ME Association: ‘ME Awareness Week 2018’ New Early Day Motion Launched by Carol Monaghan MP

http://www.meassociation.org.uk/2018/05/me-awareness-week-2018-new-early-day-motion-launched-by-carol-monaghan-mp-09-may-2018/

‘ME Awareness Week 2018’ New Early Day Motion Launched by Carol Monaghan MP | 09 May 2018

An early day motion has been launched by Carol Monaghan MP, and she needs your help in asking other MPs to sign the motion increasing the chance it will lead to an actual debate in parliament.

What is an early day motion?

Early day motions (EDMs) are motions submitted for debate in the House of Commons for which no day has been fixed. As there is no specific time allocated to EDMs very few are debated. However, many attract a great deal of public interest and media coverage.

EDMs are used to put on record the views of individual MPs or to draw attention to specific events or campaigns. Topics covered by EDMs vary widely. By attracting the signatures of other MPs, they can be used to demonstrate the level of parliamentary support for a particular cause or point of view.

What is this EDM all about?

The new EDM draws attention to ME Awareness Week and it is hoped that it will attract the signatures from those MPs who have an interest in M.E. or whose constituents have raised it as an issue with them.

Early day motion 1247

ME AWARENESS WEEK 2018

Session: 2017-19

Date tabled: 08.05.2018

Primary sponsor: Monaghan, Carol

Sponsors: Black, Mhairi ,Gibson, Patricia, Bardell, Hannah, Sheppard, Tommy, Brock, Deidre

“That this House recognises Myalgic Encephalomyelitis (ME) Awareness Week from 6 to 12 May 2018, which aims to aims to highlight the impact this invisible illness has on 250,000 people across the UK; recognises the fantastic work campaigners and charities are doing to highlight ME as a physical condition which is not all in the mind; acknowledges the detrimental effect of the PACE trials and its results, and the work which is being done to reverse this; and encourages people to go blue for ME across the week, to further bring this illness out of the shadows and into the spotlight.”

The idea is that the more signatures this EDM attracts the greater the chance of an actual debate taking place in parliament on particular issues relating to M.E. Such issues are likely to be:

Medical Education

Need for an Early and Accurate Diagnosis

NICE guideline review

The PACE trial

NHS services postcode lottery

Problems relating to children (child care facilities)

Severe ME (lack of domiciliary services and specialised units and difficulties accessing social care)

DWP benefits

Biomedical research

Write to your MP

The ME Association, #MEAction and other charities have been working together to provide a comprehensive briefing document for those MPs who are interested, and we hope that with your help we can persuade more to sign the EDM and express their interest in a further debate.

So, please write or email your MP and ask them to support this EDM explaining why, in your own words, these issues are so important. You can find your MP’s details by visiting the parliament website and entering their name or your postcode.

Your letter or email need not be long or involved. This template might help, but feel free to personalise. Some people feel that a written (even typed) letter sent in the post achieves a better result, but choose whatever means is easiest for you.

Dear (Insert MP name here),

I am writing to ask that you sign EDM 1247, in support of ME Awareness Week.

As your constituent, this issue is very important to me, and I would be grateful if you could lend your support to this EDM.

(Insert personal message)

Kind regards,

(Insert constituent name)

(Make sure to include full name and address when signing off, i.e:

Joe Bloggs

123 House Avenue

London

X12 Y34)


May 2018

Pharmacological activation of AMPK [AMP-activated protein kinase] and glucose uptake in cultured human skeletal muscle cells from patients with ME/CFS

http://www.meresearch.org.uk/our-research/completed-studies/pharmacological-activation-of-ampk/

Authors

Audrey E Brown, Beth Dibnah, Emily Fisher, Julia L Newton and Mark Walker

Institutions

Institute of Cellular Medicine, Newcastle University; Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK

Abstract

Background: Skeletal muscle fatigue and post-exertional malaise are key symptoms of Myalgic Encephalomyelitis (ME/CFS). We have previously shown that AMPK activation and glucose uptake are impaired in primary human skeletal muscle cell cultures derived from patients with ME/CFS in response to electrical pulse stimulation, a method which induces contraction of muscle cells in vitro. The aim of this study was to assess if AMPK could be activated pharmacologically in ME/CFS.

Methods: Primary skeletal muscle cell cultures from patients with ME/CFS and healthy controls were treated with either metformin or 991. AMPK activation was assessed by Western blot and glucose uptake measured.

Results: Both metformin and 991 treatment significantly increased AMPK activation and glucose uptake in muscle cell cultures from both controls and ME/CFS. Cellular ATP content was unaffected by treatment although ATP content was significantly decreased in ME/CFS compared to controls.

Conclusions: Pharmacological activation of AMPK can improve glucose uptake in muscle cell cultures from patients with ME/CFS. This suggests that the failure of electrical pulse stimulation to activate AMPK in these muscle cultures is due to a defect proximal to AMPK. Further work is required to delineate the defect and determine whether pharmacological activation of AMPK improves muscle function in patients with ME/CFS.

Publication

Brown et al, Bioscience Reports, 2018 Apr 13; Epub ahead of print

Funding

The work was funded by ME Research UK and supported by the NIHR Newcastle Clinical Research Facility.

Comment by ME Research UK

Abnormal muscle fatigue is one of the most common symptoms reported by people with ME/CFS, and can occur even after periods of only mild exercise.

Since 2006, ME Research UK has provided pilot funding for a number of projects at Newcastle University exploring the mechanisms underlying this symptom, and one key study took a close look at muscle cell function using biopsies obtained from ME/CFS patients.

These muscle cells were cultured and examined in standardised laboratory conditions by applying a series of electrical pulses to simulate the muscle contraction that occurs during exercise.

The researchers found that the activation of AMP-activated protein kinase (AMPK) and the uptake of glucose were both impaired in these cells. AMPK has an important role in regulating energy in the cell and is normally activated during muscle contraction, while glucose is an important energy source.

Although AMPK was not activated by simulated muscle contraction in these cells from ME/CFS patients, later experiments indicated that it could be activated by treatment with metformin. This raises the possibility of whether a drug such as this could improve muscle function in patients.

To look at these abnormalities in more detail, and potentially to trace where they occur in the signalling pathway, the Newcastle team began a series of experiments funded by ME Research UK.

The first part of this work, published in Bioscience Reports, used a similar methodology to that in their previous study to investigate whether AMPK and glucose uptake in muscle cells from ME/CFS patients could be activated by treatment with pharmacological agents.

Skeletal muscle cells were obtained from eight patients with ME/CFS and from seven healthy control subjects. The cultured cells were then treated with metformin or with compound 991. Metformin is a drug commonly used to treat diabetes, and is known to activate AMPK indirectly via other mechanisms. Compound 991, on the other hand, was designed specifically as a direct activator of AMPK.

Treatment with metformin increased both AMPK activation and glucose uptake, and this was true for muscle cells from ME/CFS patients and from healthy control subjects. Similarly, compound 991 treatment also significantly increased both parameters in patient and control cells, and the effect on glucose uptake was similar to that expected following treatment with insulin.

Therefore, while AMPK in muscle cells from ME/CFS patients is not activated by electrical stimulation of the cells, it can be activated pharmacologically, and there are two important conclusions that might be drawn from these findings.

Firstly, this abnormality in signalling can potentially be bypassed by pharmacological treatment, and the investigators suggest that this adds further support to the idea of conducting a clinical trial of an AMPK activator in ME/CFS patients. Secondly, their results indicate that the signalling defect lies further up the molecular chain, possibly involving upstream enzymes such as LKB1 or CaMKK.

These findings represent the fascinating first steps of this project, which will continue to look more closely at the mechanisms underlying muscle fatigue in ME/CFS, and hopefully to identify potential targets for therapy.


April 2018

I Am Stuck In The Prison That Is ME

Ellie Bunce

https://www.huffingtonpost.co.uk/entry/i-am-stuck-in-the-prison-that-is-me_uk_5acf4ab8e4b0648767777931

I had hopes of being an Olympian – now I’m bed-bound with an illness some people think doesn’t exist.

ME, two simple letters that can rip apart everything you worked for and everything you ever dreamt of.

Myalgic encephalomyelitis is a soul destroying disease that leaves so many bedridden without anyone knowing.

I’ve had ME for two years now after coming down with glandular fever in Easter 2016. At the time I was 19, a student athlete – in my second year of university – with hopes of rowing internationally. I was fit, active, I ate well, I exercised. I was happy and positive and yet one day I woke feeling as if I was dying. It was like my whole body ached, in a way I’d never felt before – I felt drained of everything I had. I knew instantly something was wrong.

After calling 111 it was thought I had meningitis and an ambulance took me to A&E where various tests showed I had nothing wrong and was sent home with a suspected viral infection. However, that evening my tonsils went bright white and swelled so much I couldn’t breathe or swallow. Again I called 111 and was sent to an out of hours doctor where I was told I had tonsillitis.

A course of antibiotics cleared up my throat but I never felt the same again. Training was hard, I was always in pain and out of breath. After a week my tonsils flared up again. This time I was told in was glandular fever and to rest.

Months and months went past and I never got better.

Eventually it was thought I had chronic fatigue syndrome (ME). Since then I’ve spiralled downhill, getting more poorly everyday. From what I know, ME is an inflammation in my brain and nervous system which has left me in excruciating chronic pain, poor cognitive function, a weakened immune system and chronically fatigued.

Day to day every inch of my body is in pain, I struggle to read and concentrate, I’m sick, I’m too tired to move, bright lights hurt my eyes, loud noises hurt my head. I spend upwards of 20 hours in bed a day in order not to “crash”. In my crashes, I scream in pain, unable to talk, or move. My whole body shakes, my eyes roll. It’s like my whole body is screaming at me to stop.

Some days, when I feel a little better for an hour or two, I’ll see a friend. I look well. Nothing looks wrong with me. They don’t see me lying in bed screaming in pain. No one understands what truly goes on behind closed doors. People will ask me if I feel a bit tired. Or stare at me if I stand up after using a wheelchair. I’m questioned if it’s my mental health. If I’m lazy.

Have you ever laid in bed and felt so ill that you truly thought you were going to die?

ME is a hugely misunderstood and unheard of illness.

For years it was misdiagnosed and not believed. I’ve struggled with various doctors not understanding the condition and suggesting treatment, which in fact, made me worse. The first ‘specialist’ I saw suggested it was my personality.

He said, I should make more effort to wake up at 9am get showered, dressed and then go on a long walk. This was my ‘treatment plan’. However, the more I pushed myself to get out of bed, the more ill I got.

Imagine how you would feel if haven’t slept in three days, you caught the flu, had the worst hangover of your life – and you had to run a marathon feeling like this. This is how I feel everyday.

Having ME can leave me feeling invisible, unheard and misunderstood. It has lead to me developing various other conditions, such as depression, anxiety, eczema, migraines and tonsillitis. Because my immune system has been weakened I also regularly get viral infections on top of this.

My mind often wonders what I wish I could do if I wasn’t ill. I am stuck in the prison that is ME. When you are stripped of your hobbies, talents, energy and work then who do you become?

ME has made me become stronger mentally. I now find joy in the little things – a cuddle with my puppy, the blue sky, the sound of birds singing, the warm sun on my face.

I extremely grateful for all my family, relatives and the close friends who understand. I know it is hard for them to see me crumble into a shell of my former self. I live in the hope that one day doctors will find a treatment, one day there will be funding for more research, and one day I will be better.

The ME Association is at the forefront of improving access to care, treatment and research and removing the disease’s stigma.

MEA medical adviser Charles Shepherd said: “Several quality of life research studies have shown that the level of disability in ME can be just as great than many other serious medical conditions, including cancer and multiple sclerosis.

“While some some people with ME do improve over the course of time, it is only a small minority that return to full normal health.

“Despite being recognised by the World Health Organisation as a neurological disease, and a report from the Chief Medical Officer of Health calling for more research and a network of hospital based clinics, many doctors still don’t know how to diagnose and manage ME/CFS and lack or research means that we still don’t have any effective forms of treatment.

“This is a completely unacceptable situation for a disease that is twice as common as multiple sclerosis and where a new report has estimated that is costing the UK economy around £3.5 billion in lost taxes, healthcare and benefit costs.”

For more information on ME, or to donate towards research, visit the ME Association website: www.meassociation.org.uk


April 2018 

Forward-ME Group Letter to the Science Media Centre, April 2018

http://www.meresearch.org.uk/news/forward-me-group-letter-science-media-group/

Forward-ME Group Letter

Forward-ME Group Chair, The Countess of Mar, has written on behalf of the members of the Group to the Chief Executive of the Science Media Centre asking for the SMC “to retract and replace your factsheet on CFS/ME, published on 21 March 2018”. The letter continues that the factsheet, entitled “CFS/ME – The illness and the controversy” “……. includes numerous inaccuracies and distortions; it denigrates patients and some doctors; it fails to reflect the numerous peer reviewed papers, published since the release of some of the raw data from the trial following legal action, which demonstrate serious defects in the PACE trial, and it fails to take into account the extensive research from the USA published since 2014. This will all have been available to you.”

The full text of the letter is as follows –

“Re: Science Media Centre Factsheet – CFS/ME – The illness and the controversy.

On behalf of Forward-ME I write to ask you to retract and replace your factsheet on CFS/ME, published on 21 March 2018, following the publication of a paper by Dr Carolyn Wilshire of the University of Wellington, New Zealand, which found that the findings of the Principal Investigators of the PACE trial were ‘not robust’ and showed ‘no long-term benefits’.

The factsheet includes numerous inaccuracies and distortions; it denigrates patients and some doctors; it fails to reflect the numerous peer reviewed papers, published since the release of some of the raw data from the trial following legal action, which demonstrate serious defects in the PACE trial, and it fails to take into account the extensive research from the USA published since 2014. This will all have been available to you.

The factsheet states: “CFS/ME is highly controversial with longstanding disagreements between the mainstream medical community and campaigners about its cause and treatment”. It also states that “amongst the mainstream medical research community, CFS/ME and NICE recommend management that is not especially controversial.

These claims are patently inaccurate. The mainstream medical community in the USA concluded that the “campaigners” have actually been correct about the nature of the condition, stating that “ME/CFS is a serious, chronic, complex systemic disease” (Academy of Medicine), that it is not a primary psychological disease in aetiology” (National Institutes of Health). They state that guidance for managing ME/CFS should include a “declaration that the disease is not the result of fear-based avoidance of activity”, and a clear indication that the disease is not a psychiatric or somatoform disorder” (Chronic Fatigue Syndrome Advisory Committee of the Department of Health and Human Services). There certainly is controversy and disagreement at this time, but that disagreement is not between professionals and “campaigners”. It is between professionals in the UK and professionals elsewhere.

The factsheet claims that: “After sustained pressure from activists the CDC has removed mention of CBT and GET from its website”. This, too, is patently inaccurate and even a cursory investigation of the facts would make that clear. The CDC changed its recommendations at the urging of the Academy of Medicine, the National Institutes of Health, the Department of Health and Human Services, and the Agency for Healthcare Quality and Research, all of whom emphatically agree that the CDC’s former recommendations – that is, the current NICE recommendations – lack evidence based support.

The author of the factsheet states that existing evidence in favour of CBT and GET is “cited by the scientific community”, as if there are no reputable members of the scientific community, and no reputable health policy authorities who disagree. They go on to state that “those who disagree …. cite review articles and reanalyses of trial data published in low impact factor journals such as The Journal of Health Psychology and Fatigue: Biomedicine, Health and Behaviour”.

It is concerning that a reputable resource like the Science Media Centre would publish such a grossly inaccurate claim, one that can be so readily overturned. Those who disagree with the evidence for CBT and GET cite the extensive investigations of the US governmental health authorities. In particular they cite the Agency for Healthcare and Research Quality Publication No. 15-E001-EF, “Diagnosis and Treatment of Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome”. That document is readily available online and a quick investigation will reveal that it offers a very long and detailed list of unscientific practices and biases in the research that claims to support CBT and GET. There are a great many such reports by US governmental health organisations. It is unacceptable for the Science Media Centre to write as if these investigations did not take place; as if these documents do not exist – and it is unacceptable not to note that, by comparison, the professional reputations of these organisations far outstrip those of the PACE trial researchers.

The reality is that at this time there are no US governmental health authorities who agree that the PACE trial is “good quality”. It is absurd for any “Factsheet” on ME/CFS to overlook this fact.

Your Trustees’ Report for the year ended 31 March 2016 gives among the SMC objectives its overall goal to help to achieve the aim of the House of Lords Science and Technology Committee which sought to renew public trust in science “by working to promote more balanced, accurate and rational coverage of the important science, health and environment stories that appear in the media.” In the case of the promotion of the science relating to CFS/ME the Science Media Centre have singularly failed in its objectives over many years.

If you are not prepared to retract this factsheet I regret that we have no option but to report our concerns to the Charity Commission.

I look forward to hearing from you shortly.

Yours sincerely

Countess of Mar

Chairman – Forward-ME

Copy to: Professor Jonathan Baker, Chair of Trustees. ”

By way of background information, the Science Media Centre (a registered charity) has as its stated mission “To provide, for the benefit of the public and policymakers, accurate and evidence-based information about science and engineering through the media, particularly on controversial and headline news stories when most confusion and misinformation occurs.”  It states that it provides “journalists with what they need in the timeframe they need it, from interviews with leading experts to timely press briefings on topical issues. We provide journalists with information about science and its related disciplines, making it easier for them to get access to the best evidence and expertise. Given our focus on science in the headlines, the SMC works mainly with science and news journalists in the UK’s national news outlets.” The Centre sends out quotes from experts, statistical analyses of scientific studies and Factsheets, in addition to running regular press briefings on the latest hot topic.


March 2018

The PACE Trial continues to unravel …

A major study has been released today (22nd March) which again looks at the PACE Trial, and this in turn has led to a lot of coverage in the media.

“The message is clear – CBT and GET are not effective ways of treating a serious neuroimmune disease. The sooner this message gets across to health professionals the better.” (Dr Charles Shepherd, The ME Association).

The study –

Rethinking the treatment of chronic fatigue syndrome—a reanalysis and evaluation of findings from a recent major trial of graded exercise and CBT

https://bmcpsychology.biomedcentral.com/articles/10.1186/s40359-018-0218-3

PDF download: https://bmcpsychology.biomedcentral.com/track/pdf/10.1186/s40359-018-0218-3?site=bmcpsychology.biomedcentral.com

Some of the media coverage –

BBC

Chronic fatigue trial results ‘not robust’, new study says

http://www.bbc.co.uk/news/health-43490335

Belfast Telegraph

Findings of chronic fatigue study ‘not reliable’
The study faced intense criticism from patients and charities

https://www.belfasttelegraph.co.uk/news/uk/findings-of-chronic-fatigue-study-not-reliable-36733161.html

Daily Mail

Findings of chronic fatigue study `not reliable´

http://www.dailymail.co.uk/wires/pa/article-5532233/Findings-chronic-fatigue-study-not-reliable.html

The Canary

The mainstream medical community just declared war on people living with ME

https://www.thecanary.co/discovery/analysis-discovery/2018/03/22/the-mainstream-medical-community-just-declared-war-on-people-living-with-me/

The Times

Findings of £5m ME chronic fatigue study ‘worthless’

https://www.thetimes.co.uk/article/findings-of-5m-me-chronic-fatigue-study-worthless-89z8x0xzr

The ME Association’s response 

Reanalysis of the PACE trial finds impressive claims for recovery following CBT and GET are ‘not statistically reliable’

http://www.meassociation.org.uk/2018/03/reanalysis-of-the-pace-trial-finds-impressive-claims-for-recovery-following-cbt-and-get-are-not-statistically-reliable-22-march-2018/

ME Association Press Release, 21st March 2018

Benefits reported in a controversial medical trial part-funded by the Department of Work of Pensions were “not reliable,” a major study has found.

A large-scale, government-funded trial, known as PACE, claimed psychotherapy and exercise helped the estimated 250,000 sufferers of the devastating illness, M.E. (myalgic encephalomyelitis).

Manifesting as unrelenting fatigue and profound pain, the condition, also known as chronic fatigue syndrome, has no known cure and is made worse by exertion.

Sufferers are often confined to their beds, unable to walk, and need help even to shower – an action that could then lay them low for hours, days, weeks or longer.

When the results of the five-year PACE trial were published in 2011, researchers claimed that graded exercise therapy (GET) and cognitive behaviour therapy (CBT) were “moderately effective” forms of treatment.

The trial concluded that both treatments led to recovery in over a fifth of patients.

But PACE has since faced intense criticism from patients and charities, such as the ME Association, over how the results were obtained, analysed and presented.

Parliament has previously heard claims that the data was deliberately flawed to “remove people from long-term benefits and reduce the welfare bill”

After a long legal battle, unpublished data from the trial was released and has now been independently reanalysed. The paper, published in the journal BMC Psychology, has found that the benefits reported for psychotherapy and exercise therapy are modest and not statistically reliable.

Lead author Carolyn Wilshire, said:

“Our reanalysis was designed to explore how the PACE trial outcomes would have looked if the investigators had adhered to the primary outcome they described in their original published protocol.

“We also looked into the published data on long-term outcomes to examine whether they had been influenced by the treatments patients had received after the trial had ended.

“We found that the groups receiving CBT or GET did not significantly outperform the control group after correcting for the number of comparisons specified in the trial protocol. Rates of recovery were consistently low and not significantly different across treatment groups.”

In surveys carried out by the ME Association, more than half of patients who had followed the recommended graded exercise programme saw a worsening in their symptoms.

Dr Charles Shepherd, Honorary Medical Adviser to the ME Association, today said:

“The ME Association has always been very critical of the way in which the PACE trial was designed, especially the lack of any objective outcome measures.

“And we have not been impressed by the way in which the results have been reported in medical journals, especially claims relating to recovery following CBT and GET.

“So, it comes as no surprise to find that a very careful re-analysis of some of the PACE trial data by Carolyn Wilshire and colleagues has concluded that impressive claims for recovery following CBT and GET are not statistically reliable.

“It is also very concerning to note that this data was only released through use of the Freedom of Information Act and a very costly Tribunal – which ordered the release of data.

“This sends a powerful message to the research community that they must be willing to share data where there are serious concerns about protocols or the reliability of results from a clinical trial.

“The ME Association believes that it is very important to encourage research data sharing and, where appropriate, independent reanalysis – which is why we made a significant financial contribution towards the processing fee for publication of this paper.

“The message is clear – CBT and GET are not effective ways of treating a serious neuroimmune disease. The sooner this message gets across to health professionals the better.”

The PACE trial data was used justify NHS recommendations of exercise and cognitive behaviour therapy and no changes were made as a result.

But a patient revolt has forced the government and NICE (the National Institute of Clinical Excellence) to review the guidelines used by UK doctors. That review may not be completed before 2020.

Forward ME Letter to The Times: Patients with ME/CFS ‘are not simply “deconditioned” as claimed by many psychiatrists’ | 23 March 2018

http://www.meassociation.org.uk/2018/03/forward-me-letter-to-the-times-patients-with-me-cfs-are-not-simply-deconditioned-as-claimed-by-many-psychiatrists-23-march-2018/

Letter to The Times, 23rd March, 2018.

Treatment for patients with M.E.

Sir,

The article by Tom Whipple, (“Findings of £5m ME chronic fatigue study ‘worthless’,” Mar 22) highlights a long-standing problem.

The National Institute for Health and Care Excellence (Nice) is in the process of replacing its guideline for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), but this will take time.

Patients with ME/CFS in this country continue to receive damaging treatment in the form of graded exercise therapy (GET). Despite evidence of disabling metabolic abnormalities in their muscles, patients are advised to “exercise back to fitness”.

They are not simply “deconditioned” as claimed by many psychiatrists. Forced exercise above very low levels characteristically incapacitates most patients.

The “exercise will make you better doctrine” applied to ME/CFS is profoundly incorrect and has no scientific evidence base.

The human cost is enormous, with many sufferers from ME/CFS rendered worse by inappropriate medical management.

Even worse, such management is inflicted compulsorily on some patients, both adults and children, with their informed consent being bypassed via the use of mental health and child protection legislation.

Signatures

Countess of Mar, Forward-ME; Dr William Weir, infectious disease consultant; Dr Nigel Speight, paediatrician; Dr Charles Shepherd, ME association; Dr Vance Spence, ME research UK; Jonathan Davies, ME research UK; Dr Gareth Tuckwell, ME trust; Dr Paul Worthley, ME trust; Jane Colby, Tymes trust; Helen Brownlie, 25 per cent ME group; Tanya and Christine Harrison, Brame; William and Janice Kent, Remember; Hannah Clifton, ME trust; Clare Ogden, Action for ME


March 2018

Higher prevalence of ‘low T3 syndrome’ in patients with chronic fatigue syndrome: A case-control study

(This very much fits in with the research showing that ME is a hypometabolic disease e.g, the research at Stanford University, California.)

https://www.frontiersin.org/articles/10.3389/fendo.2018.00097/abstract

Begoña Ruiz-Núñez 1, 2*, Rabab Tarasse 1, Emar Vogelaar 3, Janneke Dijck-Brouwer 1 and Frits Muskiet 1

1 Laboratory Medicine, University Medical Center Groningen, Netherlands
2 Healthy Institute, Spain
3 European Laboratory of Nutriënts (ELN), Netherlands

Chronic fatigue syndrome (CFS) is a heterogeneous disease with unknown cause(s). CFS symptoms resemble a hypothyroid state, possibly secondary to chronic (low-grade) (metabolic) inflammation. We studied 98 CFS patients (21-69 years, 21 males) and 99 age- and sex-matched controls (19-65 years, 23 males). We measured parameters of thyroid function, (metabolic) inflammation, gut wall integrity and nutrients influencing thyroid function and/or inflammation. Most remarkably, CFS patients exhibited similar TSH, but lower FT3 (difference of medians 0.1%), TT4 (11.9%), TT3 (12.5%), %TT3 (4.7%), SPINA-GD (14.4%), SPINA-GT (14.9%), 24-hour urinary iodine (27.6%) and higher %rT3 (13.3%). FT3 below the reference range, consistent with the ‘low T3 syndrome’, was found in 16/98 CFS patients vs. 7/99 controls (OR 2.56; 95% CI=1.00 – 6.54). Most observations persisted in two sensitivity analyses with more stringent cut-off values for BMI, hsCRP and WBC. We found possible evidence of (chronic) low-grade metabolic inflammation (ferritin and HDL-C). FT3, TT3, TT4 and rT3 correlated positively with hsCRP in CFS patients and all subjects. TT3 and TT4 were positively related to hsCRP in controls. Low circulating T3 and the apparent shift from T3 to rT3 may reflect more severely depressed tissue T3 levels. The present findings might be in line with recent metabolomic studies pointing at a hypometabolic state. They resemble a mild form of ‘non thyroidal illness syndrome’ and ‘low T3 syndrome’ experienced by a subgroup of hypothyroid patients receiving T4 monotherapy. Our study needs confirmation and extension by others. If confirmed, trials with e.g. T3 and iodide supplements might be indicated.


March 2018

DNA gets away: Scientists catch the rogue molecule that can trigger autoimmunity

(This is not specifically about ME, but may be of interest as many believe that ME may well be an autoimmune condition.)

https://www.sciencedaily.com/releases/2018/02/180222145128.htm

A research team has discovered the process — and filmed the actual moment — that can change the body’s response to a dying cell

Date: February 22, 2018

Source: Monash University

Summary: A research team has discovered the process — and filmed the actual moment — that can change the body’s response to a dying cell. Importantly, what they call the ‘Great Escape’ moment may one day prove to be the crucial trigger for autoimmune diseases like arthritis.

Full Story

A research team has discovered the process – and filmed the actual moment – that can change the body’s response to a dying cell. Importantly, what they call the ‘Great Escape’ moment may one day prove to be the crucial trigger for autoimmune diseases like arthritis.

The research team, led by Professor Benjamin Kile from Monash University’s Biomedicine Discovery Institute (BDI), has discovered – and filmed – the exact moment when DNA escapes out of the mitochondria (the organelles inside cells that produce energy) during cell death. The study, published today in the journal Science, involved major collaborators from the Walter and Eliza Hall Institute and the Howard Hughes Medical Institute’s Janelia Research Campus in the US.

Mitochondria are the ultimate double agent; they are essential to keep cells alive, but when damaged, they can trigger the body’s own immune system with potentially devastating consequences. Because the DNA inside mitochondria (mtDNA) has many similarities with bacterial DNA (they share common ancestry), the body reacts to its presence outside the mitochondria, or indeed, outside the cell, as if under attack from invading pathogens. It is a similar failure to distinguish ‘self’ from ‘non-self’ that underlies inflammatory and autoimmune diseases.

While the release of mtDNA is thought to contribute to autoimmune diseases such as lupus, how it escapes from the mitochondria has never been explained. Monash BDI researcher Dr Kate McArthur, while completing her PhD at the Walter and Eliza Hall Institute, used a revolutionary new microscope at the Janelia Research Campus in the US to capture the moment when mitochondria form a ‘hernia’ that balloons out of the mitochondria expelling the DNA into the rest of the cell.

The live-cell lattice light-sheet microscopy (LLSM) system developed by Nobel Prize winner Eric Betzig is a new technique that allows scientists to observe living cells at groundbreaking resolution. Dr McArthur travelled to the Janelia Research Campus in Virginia multiple times between 2015-2017, and remembers the moment when she witnessed, for the first time, the mitochondria actively expelling its DNA.

“As scientists, we are taught to be quite sceptical when we see something unexpected, so I think my initial reaction was ‘no way…’

“It was only after I had carefully repeated the experiment many times that I began to realise what we had found,” Dr McArthur said.

According to Professor Kile, when a cell commits suicide (a normal part of the human body’s balancing act to control blood cell numbers), two proteins called BAK and BAX are triggered.

“What we witnessed – in real time – was these professional killer proteins opening up huge ‘macropores’ in the outer membrane of the mitochondria, leading the inner contents to herniate out, bringing the mtDNA with it,” Professor Kile said.

“BAK and BAX deliver the ‘kill shot’ designed to permanently disable the cell. But in doing that, mtDNA is lost from the mitochondria. In essence, this is collateral damage, which, if it isn’t controlled properly, triggers the immune system to drive pathological inflammation,” he said.

The discovery was cemented by images captured by Monash University’s Titan Krios cryo-electron microscope, currently the most advanced microscope for biological electron microscopy, and the Walter and Eliza Hall Institute’s new lattice light-sheet microscope, custom built by collaborators in the Institute’s Centre for Dynamic Imaging.

Professor Kile stressed that, in research, “fundamental discoveries such as this are rare, and this one has profound implications for the understanding of a wide range of autoimmune diseases and infections.

“This has been a brilliant collaboration – between Monash’s Biomedicine Discovery Institute, the Walter and Eliza Hall Institute of Medical Research here in Melbourne and the Janelia Research Campus in the US – which has brought together cutting-edge technologies and first-class expertise to address questions that before now, had never been asked, and would have been impossible to answer,” he said.


February 2018

Neurologic Abnormalities in Myalgic Encephalomyelitis / Chronic Fatigue Syndrome: A Review

https://www.ncbi.nlm.nih.gov/pubmed/29348374

Komaroff AL 1, Takahashi R, Yamamura T, Sawamura M.

1 Department of Medicine, Brigham & Women’s Hospital, Harvard Medical School.

Abstract

Myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) is an illness characterized by fatigue lasting for at least six months, post-exertional malaise, unrefreshing sleep, cognitive impairment and orthostatic intolerance. ME/CFS has been a controversial illness because it is defined exclusively by subjective complaints. However, recent studies of neuroimaging as well as analysis of blood markers, energy metabolism and mitochondrial function have revealed many objective biological abnormalities. Specifically, it is suspected that the symptoms of ME/CFS may be triggered by immune activation – either inside or outside the brain – through release of inflammatory cytokines. In this review, we summarize potentially important recent findings on ME/CFS, focusing on objective evidence.

PMID: 29348374 DOI: 10.11477/mf.1416200948


February 2018

The Young ME Sufferers Trust – www.tymestrust.org

No Reported Harassment at Bristol University (Information Obtained Under FOI)

http://www.tymestrust.org/pdfs/noharassmentbristol.pdf

There has been no reported harassment of staff at Bristol University.

Yes, you read that correctly.

We have all become accustomed to the increasingly shrill ‘harassment’ accusations against ME patients and ‘activists’, both via the media and in lectures. This campaign appears to have originated at that now infamous meeting of the Science Media Centre, revealed by our original 2014 Freedom of Information Report, now updated under the title Shining a Light on the CMRC Setup(http://www.tymestrust.org/pdfs/shiningalight.pdf). Members of the UK Research Collaborative have continued to spread these allegations ever since its launch.

In Shining a Light we stated: In the records of the meeting where ‘harassment’ of researchers was discussed, no mention was made of personal threats such as have been reported in the media. Freedom of Information (FOI) requests were listed as the most damaging type of ‘harassment’. The 2016 tribunal appeal Judgement ordering QMUL to release the PACE trial data highlights that Professor Trudie Chalder accepts that “no threats have been made either to researchers or participants”.

And yet the accusations persist and have even escalated. Tymes Trust has found this constant narrative so abhorrent that we have sought some answers. We have, once again, sought evidence.

A Freedom of Information request was submitted to Bristol University, as that is where many of the accusations are coming from, to find out just how bad this claimed harassment has become. Was it just in the field of ME and CFS that this was happening, or was it more widespread?

The request was submitted to Bristol University on 19th March 2017 asking for: the number of reports of harassment that members of staff have officially recorded with Bristol University between July 2015 and January 2017. I am only interested in those reports where the harassment came from outwith the university.

Five days before the deadline for the FOI response on 13th April, the University emailed back: The University has made an initial assessment of your request, and in order to progress it further we first require clarification from you. Specifically, can you please confirm whether you require details of a third party harassing members of staff at the University, or matters where members of staff at the University have been harassed by a third party? [SIC]

Confirmation was provided on the 17th April that the harassment should be by a third party.

Bristol University finally responded to the 19th March FOI request on 9th June, stating:

We have received no recorded instances of harassment of staff by a third party between July 2015 and January 2017.

We decided that this response required further investigation and a second FOI was then submitted to Bristol University on 12th June asking: Can you please provide the number of reports of harassment that members of staff have officially recorded with Bristol University between September 2010 and June 2015? I am only interested in those reports where the harassment came from outwith the university; that is, harassment of university staff by a third party.

After the 20 day statutory deadline passed with no response, a request for an internal review by Bristol University was submitted on 11th July.

Again, no response was received from the University and on 9th August an email was sent to the Information Commissioner (ICO) requesting that the appeal process be started with regard to this failure to respond.

The ICO replied on 12th August, saying that they had: written to the public authority to provide them with a copy of your original request, reminding them of their responsibilities and asking them to respond to you within 10 working days of receiving our letter (that is, by 29 August 2017). The ICO added that if you do not receive any response within 10 working days, please contact us.

By the 30th August, one day after the 10 working day deadline, no response had been received from Bristol University and a further email was sent to the ICO advising them of this fact.

At 5.21pm that same day, Bristol University then responded to the FOI request of 12th June, stating: We have received no official reports of harassment of University staff by a third party between September 2010 and June 2015.

Conclusion

The 2016 tribunal appeal Judgement ordering QMUL to release the PACE trial data, which had found, in the Judge’s words, no threats have been made either to researchers or participants, taken together with this new information that Bristol University have no reports of harassment of University staff by a third party between September 2010 and January 2017 raises questions about such accusations and about those who make them.

Why did we use Freedom of Information?

Freedom of Information requests provide the public with access to information held by public authorities. The aim of the Freedom of Information Act was a more open government based on mutual trust.

The ICO website states that Public authorities spend money collected from taxpayers and make decisions that can significantly affect many people’s lives. The decisions and actions of researchers in the field of ME and CFS do significantly affect many people’s lives. The Government White Paper Your Right to Know: Freedom of Information 1998 stated: Unnecessary secrecy in government leads to arrogance in governance and defective decision making.


January 2018

Why study metabolomics in ME/CFS?

https://www.omf.ngo/2018/01/03/study-metabolomics-cfs/

January 3, 2018

From the Open Medicine Foundation –

Happy new year, and happy #OMFScienceWednesday! As many of you out there are recovering from the holidays, today’s topic is metabolomics. Metabolomics simply describes a way to study metabolism – that is, through measuring amounts of the metabolites (small molecules) produced by our bodies as we convert food into energy and other molecules that our cells need to survive. Metabolomics technology is ‘large-scale,’ meaning that several thousand metabolites can be measured from a single sample of e.g., blood or urine.

Metabolomics has become a very hot topic in ME/CFS research, and one that we are involved in supporting, because Dr. Ron Davis and several independent teams have used it to show metabolic differences between patients and healthy controls. This certainly makes sense based on what we know about the disease and patients not having the energy to perform the functions they always could. Metabolism is incredibly complex and can vary a lot even in healthy individuals, so it’s important to collect as much data as possible from patients. More metabolomics data will help us to understand what exactly is going wrong in ME/CFS metabolism (or if different things are going wrong in different patients), help identify metabolic biomarkers, and hopefully point to treatments that can compensate for any defects in metabolism. That’s why we are funding studies like those of Ron Davis’ lab at Stanford and Bob Naviaux’s lab at UCSD.

To learn more about metabolomics and metabolism, check out this training link.

To keep up with the latest #OMFScienceWednesday posts, follow us on Facebook.


January 2018

They told me my illness was all in my head. Was it because I’m a woman?

Why doctors must stop disbelieving women’s symptoms and institutions must do more research on diseases that primarily affect women.

https://www.bostonglobe.com/magazine/2017/12/27/they-told-illness-was-all-head-was-because-woman/47zuihgBfZqPdNe7S40hSJ/amp.html

By Jennifer Brea
December 27, 2017

Five years ago, at a restaurant in Cambridge, my waitress brought me the check. I stared at the signature line, pen in hand, and froze. I was 28 years old, a Harvard PhD student studying political economy and statistics, and I had forgotten how to write my own name.

More than a year before, my temperature had spiked to 104.7. I thought I had a bad flu. After the fever subsided, I kept getting common ailments: sore throats, sinus infections, low-grade fevers. Except I would wind up in bed, inexplicably dizzy, for days on end. After the restaurant incident, I got to the point where I could leave my house only in a wheelchair. Some days, I did not have the strength to lift my head.

Seeking answers, and care, I would eventually see a dozen specialists at Massachusetts General Hospital and Brigham and Women’s. All of their tests came back normal. As my symptoms grew in complexity, my doctors started to use words like “anxiety” or “depression.” On instinct, I started taking my then fiance, now husband, Omar, to my appointments. (I thought I might be treated better if I had a male witness.) Then a neurologist gave me a diagnosis: Conversion disorder, which prior to 1980 was called “hysteria.”

In other words, it was all in my head.

So I tested the hypothesis, walking the mile from the clinic to home, ignoring the pain in my legs. Once home, I collapsed. My brain and my spinal cord felt like they were burning. I was bedridden for months, and have never been the same since.

It turned out I have myalgic encephalomyelitis, ME, more commonly called chronic fatigue syndrome. An estimated 1 million Americans have it. Twenty-five percent are homebound or bedridden and 75 percent can’t work. And yet every day I hear from patients with ME who struggled to receive a diagnosis. On average ME patients need five years to get diagnosed, and many sufferers report spending much of that time being told their symptoms are psychological. In general, women are 2 to 10 times more likely than men to receive a diagnosis of hysteria. And while globally, ME affects millions of men, 80 percent of people who have it are women.

The phenomenon of disbelieving women’s symptoms extends far beyond ME. Forty-five percent of patients with autoimmune disorders — the majority of whom are women — are initially told they are hypochondriacs before being accurately diagnosed.

We endure such waits, I believe, not because my disease is inherently inscrutable but because we have chosen not to invest in understanding it. For more than a decade, ME has received just $5 to $6 per patient annually in research funding from the National Institutes of Health, the second lowest of any disease for which NIH reports categorical funding. (The lowest, fibromyalgia, has a patient population that is 90 percent female.) Less than a third of medical schools even incorporate ME into their curricula. You cannot find answers to the questions you don’t ask — or don’t fund.

Here’s what we do know: The disease is frequently triggered by an infection, and many symptoms, including dizziness, appear or worsen when a person stands up (doctors call this orthostatic intolerance). ME patients have immune abnormalities, and some may have an autoimmune disease. We also have a defect that limits our metabolic ability to convert sugar into energy. ME’s hallmark feature is “post-exertional malaise” — after cognitive or physical exertion, every system of the body is affected so severely by symptoms that we call it a “crash.”

I’m lucky. I got diagnosed and have improved with treatment. I was able to give a TED Talk and, from bed, make a documentary, Unrest, about my experience. I can leave my house now, albeit in a wheelchair. But complete recovery from ME is rare.

When I first got sick, I thought maybe I had a rare disease — something doctors had simply never seen. Then I came to understand I was part of a community of millions living with ME who had been systematically disbelieved and marginalized. What I now know is that around the world, hundreds of millions live with autoimmune diseases. These are often complex, difficult-to-diagnose conditions that modern medicine is ill-equipped to treat. They disproportionately affect women and their incidence is rising. We need to band together across the borders of our diagnoses to build a movement for more investment in research and better care.

And in the meantime, it’s important that doctors tempted to offer a patient a psychological cause for their symptoms stop and ask themselves about the assumptions they might be making based on gender. Conversion disorder affects perhaps 14 to 22 people out of 100,000, so the chances a doctor will ever see a patient with it are not high. It would be far better, when confronted with a puzzle that defies diagnosis, to say, “I don’t know.” For patients like me, those words can be as lifesaving as medicine.

Jennifer Brea is a health activist and filmmaker whose 2017 documentary, “Unrest,” is on the short list for an Academy Award It premieres on PBS January 8.


December 2017

ME/CFS Collaborative Research Center at Stanford University, funded by OMF

https://www.omf.ngo/collaborative-research-center-stanford/

The ME/CFS Collaborative Research Center at Stanford will be led by Dr. Ron Davis, Professor of Biochemistry and Genetics at Stanford University, and Director of our Scientific Advisory Board. Dr. Davis has assembled a truly world-class team of researchers, many of whom have never before focused their expertise on ME/CFS, and has planned several innovative projects that will help us to understand the molecular basis of ME/CFS, develop better diagnostics, and discover new treatments. Given the number and quality of investigators that this grant would bring into the field, and the likelihood of groundbreaking discoveries coming from this research, OMF has decided to fund this highly promising proposal. Although the National Institutes of Health decided against funding this plan as one of their Collaborative Research Centers, we believe this work is too important and too promising not to pursue. We are not willing to miss the opportunity to actively involve a scientific team of this caliber in the field of ME/CFS research. OMF will, therefore, be supporting the first year of this groundbreaking research with $1.2 million, and we are actively and enthusiastically raising the funds needed to support the remaining 4+ years it will take to complete it.

Scientific Plan

The Center will pursue three distinct projects, all related to understanding and treating ME/CFS by developing and using cutting-edge technologies. This work will build on previous projects that OMF has supported. For more information about these projects from the scientists involved, please see the YouTube videos from our recent Community Symposium on the Molecular Basis of ME/CFS.

1. T cells and the molecular immunology of ME/CFS

Sequencing single T cells and discovering their targets

Many studies have shown that the immune system is affected in ME/CFS patients, e.g., low activity of NK cells, altered levels of cytokines (signaling molecules of the immune system), and the likelihood of a microbial infection preceding the illness. Now, scientists on this team have implicated T cells – the immune cells responsible for identifying and killing infected cells – in ME/CFS. Specifically, their discovery of T cell clonal expansion indicates that patient T cells are reacting to a foreign invasion (e.g., virus) and/or to the ‘self’ (autoimmunity). HLA genes play a part in this reaction, and personal variations in these genes may also be playing a role in the risk of developing the disease. Discovering what is triggering this T cell clonal expansion will help to determine immunological causes of ME/CFS, may explain the elevated cytokine levels, and could lead to new treatments.

The Collaborative Research Center at Stanford will investigate the immunological basis of ME/CFS using several approaches. Dr. Mark Davis’ team will investigate the clonal expansion of T cells in ME/CFS, including what they might be targeting – viruses, bacteria, or self (autoimmune). Dr. Ron Davis’ team has invented a highly accurate, cost-effective method for HLA gene sequencing and a very sensitive method for detecting viral DNA as a sign of viral infections, which he will use in this project. Dr. Lars Steinmetz’ team has developed effective methods for sequencing RNA from single T cells, which they will use to understand how T cell behavior may be different in ME/CFS. Overall, these methods will help to determine if ME/CFS is an autoimmune disease, and what immune factors may be triggering ME/CFS or sustaining it as a chronic disease. By helping to understand the immunology of ME/CFS, it may be possible to identify treatments that modulate the immune response.

2. Extended big data study in families

Genome sequencing, gene expression, metabolomics, cytokines, clinical features, and more

OMF has funded a big data study of 20 severely ill ME/CFS patients, encompassing a huge variety of molecular and clinical tests, the largest of its kind in this disease. Among many things, this study is helping to look for genetic factors and potential molecular biomarkers, and is allowing us to generate many hypotheses. The analysis of this dataset, led by Dr. Wenzhong Xiao, has yielded many interesting observations, but it is clear that more patients must be profiled in this way to validate and extend these observations to a less severe population. The Collaborative Research Center at Stanford will expand this big data study to patients of varying severities and their families.

It has been clear for some time that there are families with multiple members affected. This might be caused by a genetic predisposition to the disease. Studying these families is likely to yield a better understanding of the factors that make someone susceptible to ME/CFS. Fereshteh Jahanbani, PhD, a Research Associate with Mike Snyder, PhD, hypothesizes that using unaffected members of these families as controls will reduce the variance in the data between controls and affected, because of the similarities in their genetics, environment, and diet. The team anticipates that this study will help define meaningful subgroups of patients, biomarkers that could be useful in diagnosis and monitoring of disease progression, and molecular defects that could be targeted with new treatments.

3. Developing blood-based diagnostic and drug screening technology

Enabling fast, inexpensive diagnosis of ME/CFS and discovery of new treatments

One of the greatest obstacles in ME/CFS research and patient care is the lack of a biological diagnostic. Dr. Davis’ engineering team has promising preliminary technologies that can distinguish ME/CFS blood samples from healthy samples, and is currently refining these technologies and investigating what the results tell us about ME/CFS biology. The technologies include the nanoneedle biosensor, developed by Rahim Esfandyarpour, PhD, the magnetic levitation platform developed by Gozde Durmus, PhD, and more. The Collaborative Center will continue this work to engineer a blood-based diagnostic device that would also be useful as a reporter for drug screening. Dr. Davis’ team has already tested chemicals in two of our platforms, some of which have made the patient samples behave more like healthy samples. To validate these findings and test large numbers of samples and candidate drugs, they will further develop and optimize the technology. Eventually, the developed technology will be shared across the ME/CFS research community to accelerate its evaluation and adoption as a clinical diagnostic assay. The Stanford Genome Technology Center has developed a number of diagnostic assays that have been commercially exported and are now in clinical use. Dr. Davis’ team has experience in the complex process of developing and implementing an assay that becomes approved for clinical use, in the USA, as well as in Europe and other countries.

Scientific Team

To carry out this ambitious work, Dr. Davis has assembled a team of extraordinary scientists with expertise in a variety of areas directly relevant to ME/CFS research. Most of these scientists are new to ME/CFS, bringing with them extensive knowledge and perspective from other fields and diseases.

ME/CFS Collaborative Research Center at Stanford Team:

Ron Davis, PhD, Professor of Biochemistry and Genetics, Stanford University School of Medicine; Director, Stanford Genome Technology Center; Director, Chronic Fatigue Syndrome Collaborative Research Center at Stanford University; Director, Open Medicine Foundation ME/CFS Scientific Advisory Board.

Mark M. Davis, PhD, Director, Stanford Institute for Immunology, Transplantation and Infection (ITI); Professor of Microbiology and Immunology; Howard Hughes Medical Institute Investigator.

Mike Snyder, PhD, Chair, Stanford Department of Genetics; Director, Stanford Center for Genomics and Personalized Medicine

Wenzhong Xiao, PhD, Director, Immuno‐Metabolic Computational Center, Massachusetts General Hospital, Harvard Medical School.

Craig Heller, PhD, Professor of Biology, Stanford University, exercise physiologist.

Robert Phair, PhD, Chief Science Officer, Integrative Bioinformatics, Inc..

Lars Steinmetz, PhD, Co-Director, Stanford Genome Technology Center; Professor of Genetics, Stanford University; Senior Scientist, Genome Biology Unit, European Molecular Biology Laboratory.

Raeka Aiyar, PhD, Director of Communications and Development, Stanford Genome Technology Center.

Laurel Crosby, PhD, Engineering Research Associate, Stanford Genome Technology Center – multi-system integration

Rahim Esfandyarpour, PhD, Engineering Research Associate, Stanford Genome Technology Center – electrical engineering, device fabrication

Fereshteh Jahaniani, PhD, Research Associate, Stanford Center for Genomics and Personalized Medicine – multi-omics

Mohsen Nemat-Gorgani, PhD, Life Science Research Scientist, Stanford Genome Technology Center – protein biochemistry, enzymology

Peidong Shen, PhD, Research Associate, Stanford Genome Technology Center – biochemistry, cell-free DNA detection methods

Gozde Durmus, PhD, Postdoctoral Fellow, Stanford Genome Technology Center – magnetic levitation platform, bioengineering

Julie Wilhelmy, Life Science Research Professional, Stanford Genome Technology Center – experimental genomics, immunology

Robert Naviaux, MD, PhD, Professor of Medicine, Pediatrics, and Pathology, University of California, San Diego; Co-Director of Mitochondrial and Metabolic Disease Center

William Robinson, MD, Associate Professor of Medicine (Immunology and Rheumatology), Stanford University

Curt Scharfe, MD, Associate Professor of Genetics, Yale University

Lucinda Bateman, MD, founder and Medical Director of the Bateman-Horne Center for ME/CFS and Fibromyalgia

David Kaufman, MD, ME/CFS Physician

Working Group

We are fortunate that many members of the scientific, medical, and biotechnology communities have offered their expertise and resources to this Center.

Paul Berg, PhD, Professor of Biochemistry, Emeritus, Stanford University; Nobel Laureate

Mario Capecchi, PhD, Professor of Human Genetics and Biology, University of Utah; Nobel Laureate

Baldomero Olivera, PhD, Professor of Biology, University of Utah

Alain Moreau, PhD, Professor of Biochemistry and Molecular Medicine, University of Montreal

Øystein Fluge, MD, Department of Oncology and Medical Physics, University of Bergen, Haukeland University Hospital, Bergen, Norway

Olav Mella, MD, Department of Oncology and Medical Physics, University of Bergen, Haukeland University Hospital, Bergen, Norway

Jonas Bergquist, MD, PhD, Professor of Analytical Chemistry and Neurochemistry, Uppsala University, Sweden

Jonas Blomberg, MD, PhD, Professor of Clinical Virology, Emeritus, Uppsala University, Sweden

Maureen Hanson, PhD, Professor of Molecular Biology and Genetics, Cornell University

Chris Armstrong, PhD, Department of Biochemistry and Molecular Biology; Bio21 Molecular Science & Biotechnology Institute researcher at the University of Melbourne, Melbourne, Australia

Neil McGregor, BDS, MDSc, PhD, senior researcher, Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, Melbourne, Australia; Adjunct Professor, Victoria University, Melbourne, Australia

Ronald Tompkins, MD, ScD, Professor of Surgery, Harvard Medical School; Founding Director of Center for Surgery, Science & Bioengineering at Massachusetts General Hospital

Catherine Blish, MD, PhD, Assistant Professor of Medicine and of Immunology, Stanford University

Christopher Garcia, PhD, Professor of Molecular and Cellular Physiology, Stanford University

Roger Howe, PhD, Professor of Engineering, Stanford University; Director, Stanford Nanofabrication Facility

Tom Soh, PhD, Professor of Electrical Engineering, Radiology, and by courtesy, Chemical Engineering, Stanford University

Robert Tibshirani, PhD, Professor of Biomedical Data Sciences and Statistics, Stanford University

Alan Light, PhD, Professor of Anesthesiology, University of Utah

Emmanuel Mignot, MD, PhD, Professor of Sleep Medicine and of Psychiatry and Behavioral Sciences, Stanford University; Director of Stanford Center for Sleep Sciences and Medicine

Gerald Shadel, PhD, Professor of Pathology and Genetics, Yale University; Director of Yale Center for Research on Aging

Jarred Younger, PhD, Associate Professor of Anesthesiology and Rheumatology and of Psychology, University of Alabama at Birmingham; Director, Neuroinflammation, Pain, and Fatigue Laboratory

John Ryals, PhD, President and CEO, Metabolon

Chunlin Wang, PhD, Chief Technology Officer, iRepertoire, Inc.

Michael Mindrinos, PhD, President of Sirona Genomics, an Immucor company

David Bell, MD, ME/CFS Physician

Kevin Tracey, MD, Professor of Neurosurgery and Molecular Medicine, Hofstra Northwell School of Medicine

Jennifer Frankovich, MD, Clinical Associate Professor of Pediatric Rheumatology, Stanford University

Jose Montoya, MD, Professor of Medicine, Stanford University; ME/CFS Physician

Susan Levine, MD, ME/CFS Physician

Harry Greenberg, MD, Senior Associate Dean of Research, Professor of Medicine, Stanford University

Bela Chheda, MD, ME/CFS Physician

Patient partners

We are very grateful for the support and contributions of the ME/CFS patient community, which has and will continue to play an integral role in moving research forward. We are committed to continuing to involve patients as participants and consultants throughout these projects, and maintaining open communication about our findings through a variety of venues. We are especially grateful to all the patients who selflessly volunteer to be subjects in our research, who generously donate to make our research possible and who send Dr. Davis their ideas, scientific analyses, and links to publications. Our patient partners are a significant and essential part of our team.


December 2017

Professor Malcolm Hooper – Off the PACE

At a conference in November run by the Academy of Nutritional Medicine (http://aonm.org/) entitled “Waking to a New Dawn: The Emergence of 21st Century Acquired Immune Deficiences & Innovative Solutions”, the keynote speaker was Professor Malcolm Hooper, who is well known to people with ME, and who gave a talk called “OFF THE PACE: CMIs, BPS, PACE, GUIDELINES and CONSEQUENCES”.

To view the PowerPoint presentation of Professor Hooper’s talk –

http://aonm.org/wp-content/uploads/2017/11/Prof.-Hooper-Off-the-PACE-CMIs-BPS-PACE-Guidelines-and-Consequences.pdf

To read his notes –

http://aonm.org/wp-content/uploads/2017/11/OFF-THE-PACE-etc-FNL.pdf

Well worth looking at by anyone interested in the background of all that has happened in the ME world over the last 30 years or so, and in finding out how things have ended up as they are now.


November 2017

Will The UK Establishment Finally Stop Denying The Reality Of ME?

http://www.huffingtonpost.co.uk/dr-simon-duffy/uk-establishment-me_b_18375968.html

By Dr Simon Duffy, Director of the Centre for Welfare Reform

Jennifer Brea’s powerful film Unrest exposes the reality of Myalgic Encephalopathy or ME. This condition leaves people utterly exhausted, or as Brea puts it, like a broken battery, unable to charge beyond 10%.

ME is poorly understood and receives minimal research. Brea was repeatedly misdiagnosed and, on one occasion, even told that it was all in the mind – the result of some long-forgotten trauma.

Eventually Brea discovered that there was not only a name for her condition but that there are millions of other people suffering with ME. With the correct diagnosis she has managed to reduce the impact of ME on her life, but she also came to understand how this real disease creates double-barrelled suffering: first, it devastates your life by robbing you of energy; second, the failure of society to respect the reality of your illness makes you invisible and defenceless.

So, why has ME been so badly misunderstood?

Dr Charles Shepherd explains that in the UK two psychiatrists played a particularly damaging role, by treating an outbreak of ME (within a hospital) in 1955 as an example of hysteria. This dangerous desire to solve a problem by evading the problem, has been made all the easier by the emergence of something called the biopsychosocial (BPS) model: this is an all encompassing framework for rethinking illness – making it part biological, part mental, part social. This may seem reasonable, but it easily becomes a way of blaming the victim and claiming it’s all in the mind.

The PACE Scandal also demonstrates the powerful forces at work. PACE was a research programme to test two ‘therapies’ for people with ME – Cognitive Behaviour Therapy (CBT) and Graded Exercise Therapy (GET). Although these therapies did not prove effective, researchers amended the rules of the evaluation so that people who had got worse were counted as having benefited from these therapies.

Outside the UK the PACE research has been severely criticised; but the Countess of Mar believes that the UK media has been frightened into silence by the Science Media Centre whose board membersinclude Sir Simon Wessely, one of the psychiatrists connected to the PACE scandal. Even more disturbing is that Mrs May has now asked Wessely to lead an Independent Review of the Mental Health Act 1983 – a decision heavily criticised by independent advocates.

The UK Government also seems to have a stake in maintaining the belief that ME is all in the mind. Mo Stewart, in her book Cash Not Care, has shown how the US Insurance Company Unum has promoted the BPS model within the DWP, encouraging the UK Government to reduce disability benefits in order to grow the market for their own disability insurance products. Lord Freud cited the PACE research as important evidence to justify the use of BPS in their welfare ‘reforms’ and medical diagnoses have now been replaced with dubious catch-all assessments of ‘readiness for work’ or ‘level of help.’ The film I, Daniel Blake accurately captures many of the horrors of these mindless and inhuman processes.

Fortunately, in the USA, researchers are now taking ME seriously, and making important progress. CBT and GET are no longer recommended as helpful therapies and instead there is increasing recognition that excessive exercise can be extremely dangerous. The level of research is still inadequate, but no one doubts the reality of the illness and important and revealing tests have been developed.

Brea’s film, which is winning awards and being widely seen, may help undermine the resistance of the UK establishment, but there is still a long way to go. Even if there are research breakthroughs people will still be living with the disabling consequences of ME. It is for this reason that the Centre for Welfare Reform is supporting the Chronic Illness Inclusion Project. Our aim is to help the community of people suffering from chronic illnesses (including, but going beyond, ME) to find their own voice, to build alliances with other disabled people and to ensure that they are no longer invisible before the eyes of the powerful.


November 2017

ME sufferers being shamefully let down by professionals

http://www.morningstaronline.co.uk/a-bd8f-ME-sufferers-being-shamefully-let-down-by-professionals#.WfQxjGiPLIU

LINDA BURNIP and DENISE McKENNA from Disabled People Against Cuts spotlight how people with ME are having their health and welfare harmed by poor research and misuse of statistics

LAST week, over 65 deaf and disabled people’s organisations, campaigns and mental health professionals wrote to the Prime Minister asking her to urgently rethink her decision to appoint Professor Sir Simon Wessely to lead the much-anticipated independent review of the Mental Health Act as announced in her speech at the Conservative Party conference on October 4.

Wessely’s body of work on myalgic encephalomyelitis (also known as chronic fatigue syndrome), and his conduct in relation to people with ME, make him resoundingly unfit to lead an inquiry into the Mental Health Act.

ME is a poorly understood illness, believed by most researchers in the field to have a physical cause. But the “psychiatrisation” of ME through a cognitive-behavioural approach to the illness led by Wessely since the late 1980s has resulted in treatment (particularly graded exercise therapy, or GET) which can be harmful and even coerced, in the stigmatisation of patients and let to the frequent denial of their entitlement to social security and support.

Wessely has consistently promoted the unsubstantiated suggestion that ME is caused or maintained by patients’ false illness beliefs and abnormal behaviour.

As a result, the integrity of patients’ experience of this devastating illness been destroyed as their testimony is deemed unreliable.

This form of “epistemic injustice” (according to medical ethics scholars Blease et al) has seen people with ME derided within the medical profession and wider society for misperceiving, exaggerating, even creating their own illness.

Wessely’s approach to ME involves treatment with GET, aimed at reversing the physical consequences of what he sees as their dysfunctional behaviour.

Nearly 50 per cent of people with ME surveyed reported that treatment with GET made their condition worse.

Yet Wessely and his colleagues are silent on the subject or dismiss patient experience as unreliable evidence or poor treatment compliance.

As a result, thousands of people with ME have received NHS treatment informed by his model that has further damaged their health.

Wessely continues to defend the notorious Pace trial, a study into CBT and GET treatment for ME/CFS part-funded by the Department for Work and Pensions and widely condemned by academics for misuse of statistical methods in order to produce positive-looking results.

Wessely’s involvement in media discussions about ME has further suppressed patients’ voices. Following the publication of results from the Pace trial, Wessely and his colleagues responded to concerns about their work by taking part in media campaign which promoted prejudice and led to those patients who had identified serious methodological and statistical problems being dismissed as irrational extremists motivated by anti-psychiatry.

The Science Media Centre, for which Wessely is a trustee, has played a key role in promoting misleading information about the Pace trial, and smearing critics.

During the 1990s Wessely advised the DWP (then DSS) that classifying ME as a neurological illness, as the World Health Organisation does, would perpetuate patients’ false beliefs, prolong their illness and result in a deluge of disability claims.

The influence of Wessely and his colleagues on DWP training manuals on CFS/ME has undoubtedly resulted in a disability assessment system biased against people with ME and caused them great additional difficulty in accessing support with the extra costs of their disability.

The work of Jonathan Rutherford reveals how Wessely was among a group of medical and insurance industry professionals whose work on “malingering and illness deception” influenced the DWP’s understanding of ill-health and disability.

Wessely and his colleagues shaped the ideology underpinning the disastrous work capability assessment (WCA) known as the “biopsychosocial model.” According to Professor Tom Shakespeare and colleagues who have exposed the poor science underpinning the biopsychosocial model, this approach to disability effectively blames disabled people seeking social security support for their own misfortune.

The WCA has had a devastating impact on the lives of disabled people as part of a package of welfare reforms leading, in the words of the UN disability committee, to “human catastrophe.”

All of these activities amount to an abuse of power by Wessely against people with ME. His thoughts and actions have led to stigma, iatrogenesis and a denial of their rights to support, all of which have compounded the burden of this illness immeasurably.


October 2017

UK ME/CFS Biobank team receives largest ever grant to continue biomedical research project

http://www.meassociation.org.uk/2017/10/uk-mecfs-biobank-team-receives-largest-ever-grant-to-continue-biomedical-research-project-30-september-2017/

Breaking News! UK ME/CFS Biobank team receives largest ever grant to continue biomedical research project

By Russell Fleming, Content Manager, ME Association.

ME Association trustees and staff were over the moon when we heard that the CureME team at the London School of Hygiene and Tropical Medicine had received a new grant of $2.1 million from the National Institutes of Health (NIH) in America.

The funding represents the biggest ever single investment in biomedical research to happen in the UK and it will enable a current project, that is searching for disease biomarkers, to be extended for another 4 years – until 2021.

The project is a longitudinal study that is measuring changes in the immune system and genetic profile of individuals in a disease whose symptoms are known to fluctuate over time. The initial £1 million project, which began in 2013, was over 3 years and had also been made possible by funding from NIH.

Dr Luis Nacul, who leads the CureME team, is also responsible for overseeing the UK ME/CFS Biobank, which has been built and maintained by charity support and the funding from America.

The new grant will enable the Biobank to increase in size as even more blood samples and clinical data will be collected from people with ME/CFS, multiple sclerosis, and healthy controls, and then made available to research applicants.

“The new grant from the NIH (US) will enable, for the first time, comprehensive prospective assessments of cases of ME/CFS at regular intervals.

“This greatly enhances the chances of a breakthrough in the understanding of the pathophysiology of this complex disease and the identification of much-needed biomarkers for the diagnosis of different sub-groups of patients.

“We very much look forward to continuing our partnership with the patient community, which has been key to the success of our research so far.”

Dr Luis Nacul, Principle Investigator, CureME team, LSHTM.

The Biobank is the only resource in the world able to include samples from those most severely affected – the house- or bed-bound – and is the premier resource outside the United States for the study of the disease. All participants are examined by a clinician and must conform to the Biobank’s rigorous protocols.

The ME Association has been a long-time supporter of the Biobank and provides funding to support its development. This longitudinal project, that in total will amount to some £2.56 million, represents one of the most exciting opportunities to learn more about this devastating disease.

Dr Charles Shepherd, Hon. Medical Adviser to the ME Association, and Chair of the UK ME/CFS Biobank Steering Group, commented:

“This is a significant and vital sum of money that will help scientists unravel the mysteries of this devastating illness.

“The irony is that the funding comes once again from America.

“What this seems to suggest is that the USA is far more serious about finding the underlying causes of M.E., while the UK seems most willing to invest in inappropriate studies using cognitive behavioural therapy and graded exercise.

“The fact that the NIH has decided to provide another major grant is an important endorsement of the ME/CFS Biobank, and we would like to congratulate all the staff who have been involved in setting up and developing what has become a vital new part of biomedical research infrastructure here in the UK.

“We hope that other research groups will also now start to make use of this unique resource to achieve desperately-needed breakthroughs into the cause and treatment of ME/CFS.

Dr Charles Shepherd, Hon. Medical Adviser, ME AssociationChair of the UK ME/CFS Biobank Steering Committee.

Research: A longitudinal immunological study for ME/CFS biomarker discovery

What are the UK ME/CFS Biobank team proposing to do with this funding?

They will be studying 110 ME/CFS cases (half severe, half mild-moderate) meeting all of the CDC, Canadian Consensus, and Institute of Medicine, criteria.

They will focus on detailed immunological and clinical phenotypes (subgrouping patients by immune differences, such as the number of different immune cells and cytokines, and clinical differences, such as severity).

Analyse inter-relationships (the relationship between the immune differences and differences in severity/symptoms and changes over time).

Cases will be assessed every 6-12 months, over 5 time points, to record changes in biomarker expression and link these to clinical parameters (whether their condition has gotten better, worse or remained stable) in order to analyse biomarkers at different stages of disease progression and try to identify subgroups.

Cases will be grouped according to trends in symptom severity using scores relating to pain, fatigue and functional status.

In-depth Immunological Profiling (to try and identify biomarkers) will involve:
* Phenotyping Lymphocytes (T cells, B cells and NK cells) and monocytes from the blood samples.
* Measuring the functional response of NK (natural killer) and T cells after stimulation (by a virus, for example).
* Analysing secreted cytokines from the stimulated NK and T cells.
* Genotyping the donors for MHC class 1 (molecules that trigger an immune response to a specific toxin or foreign substance) and KIR (recognise MHC class 1 cells and activates the killing response of NK cells).

They then want to determine whether changes in immune parameters come before, after or predict the changes observed in clinical presentation (changes in symptoms and severity over time).

This will be done by quantifying correlations between immunological biomarkers and by identifying biomarkers associated with changes in ME/CFS clinical status.

Significance of the study

“This study is unique for its strict inclusion criteria and detailed clinical phenotyping, adding specificity and validity to our analysis.”

“This is, to our knowledge, the first long-term prospective study of ME/CFS to incorporate both ambulatory and severe cases and to include comprehensive clinical data and in-depth immunological profiling.”

“This research will contribute to the development of better diagnostic tools and treatments.”

“The inclusion of severe cases through home visits will allow for research on a subset of patients often neglected in ME/CFS studies.”

“Because 1- 2.5 million Americans have ME/CFS, this study has the potential to improve the lives of a large patient population in the U.S. as well as advance the state of the field in the U.S. and internationally.”

“Patients and stakeholders are involved in all aspects of the research.”

More study information, here.

More Reaction

“This is great news for quality research into ME/CFS. The Biobank team has always put the needs of the patient first and it’s fantastic that their good work can now continue”

Cecilia Finnerty, Patient Representative.

“Such wonderful news for people with ME. It is a privilege to serve on the Steering Committee alongside a committed professional team who have such a heart for people with this illness.”

Hannah Clifton, Director, The ME Trust.

“ME Research UK is delighted that the team has been awarded a new grant from the NIH worth $2.1m. The funding will enable further research on those affected by ME/CFS over the next 4 years and will ensure that the UK’s first biobank of human blood samples continues to be a valuable resource for all researchers in the UK and beyond.”

Sue Waddle, Vice-Chair, ME Research UK.

“Congratulations to the London School of Hygiene & Tropical Medicine team for their grant award from the NIH. This is the most important development in UK research into ME this year and all the more so because it shows the international standing of the group. Very well deserved.”

Professor Jonathan Edwards, Emeritus Professor of Connective Tissue Medicine, University College London


October 2017

Individual Community Symposium talks available on the Open Medicine Foundation (OMF) YouTube Channel

http://www.meaction.net/2017/09/29/individual-community-symposium-talks-available-on-omf-youtube-channel/

The individual talks from August’s Community Symposium on the Molecular Basis of ME/CFS are now available as separate videos in a playlist on OMF’s YouTube channel.

Have a look to check out the speakers you are interested in hearing from, or the panel discussions where they answer questions from our worldwide audience.

The DVDs will be available soon and can still be ordered here.

Visit our website to learn more about the Symposium and OMF’s research.

From the OMF YouTube channel playlist –

The Community Symposium on the Molecular Basis of ME/CFS, sponsored by OMF, took place on August 12, 2017 at Stanford University. It brought together hundreds of researchers, clinicians, patients, caregivers, families, and advocates, and thousands more by livestream.

For more about the symposium, check out the following summaries:
https://www.omf.ngo/2017/08/25/community-symposium-highlights/ (shorter)
https://www.omf.ngo/2017/09/11/the-first-community-symposium-on-the-molecular-basis-of-mecfs/(more details)

To support ME/CFS research, please donate today:
https://app.etapestry.com/onlineforms/OMF/Collaborator.html


September 2017

When you beckon lightning and invite it in for tea

http://www.jkrowbory.co.uk/2017/09/when-you-beckon-lightning-and-invite-it-in-for-tea/

by Jenny Rowbory

By February 2007, I had been receiving daily Nexavir injections (an antiviral) for six months and I was actually starting to see small improvements in my health for the first time in over two years of being acutely ill. But friends and relatives kept sending me newspaper cuttings of articles about the Lightning Process (LP) curing people with ME. I became under enormous pressure to do the LP (“What’s the harm in trying it?” “Don’t you want to get better?” “It has helped others so it’s worth a shot”). I was only 20 years old, vulnerable because of my desperation to get better, and didn’t know much about Myalgic Encephalomyelitis and what the illness actually was (a multi-systemic, neuroimmune illness). By that time, I also had been gaslighted by so many NHS doctors and private doctors about my illness and symptoms, that I was doubting myself. When so many people disbelieve you, you start disbelieving yourself, despite all physical evidence to the contrary. In the end, I buckled and, although sceptical, I agreed to do the LP. I was so ill and I just wanted to get better.

Ironically, I wouldn’t have even been able to get to the LP practitioner’s house (he was an NHS doctor but did the LP privately) even a couple of months previously but because of the small improvements due to the Nexavir injections, I was able to get down the stairs and lie down in the back of our car to get there. There were consequences for my body but I thought that it would be worth it.

I’m not going to go into detail about the “mechanics” of the LP; other people have debunked the methods far better than I’m currently able to. Back then, I decided to throw myself into the LP and be totally committed to doing it properly. The results, however, were nothing less than disastrous for me.

First, the fully-qualified practitioner artfully gaslighted us (a group of four patients) with what I now know is pseudoscience quackery about M.E.; it was done in such a subtle, convincing and skilful way (even experienced scientists have been taken in by it). Using “science” to explain, he told us how we didn’t ‘have’ an illness but that we were ‘doing’ an illness; it was our thoughts, behaviours, and fears about post-exertional symptoms that were causing us to stop ourselves from living normally and causing us to believe that we had symptoms and to believe that we were ill.

He then put mechanisms into place in my brain, via neuro-linguistic programming, that made my own brain automatically gaslight me constantly and stop any thoughts of symptoms dead in their tracks. He added repetitive gestures/movements/phrases that I had to continually apply to my thoughts and body in order to reinforce the programming. This is brainwashing.

It’s hard to describe being brainwashed. The next six months in 2007 after the LP are still a hazy blur to me. Not only did the neuro-linguistic programming in my brain not allow me to ever mention any symptoms to anyone, I was not even allowed to think that I had any symptoms. I wasn’t allowed to be ill anymore. I pushed and pushed myself, even when in the most excruciating pain, even when I was in heart failure or experiencing seizures or passing out, because they didn’t exist. My illness didn’t exist [even though I was extremely ill, I honestly believed that I wasn’t ill anymore, that I was cured]. It sounds ridiculously idiotic but that’s what brainwashing can do. My body was becoming more and more damaged from the enforced gradual Graded Exercise Therapy that the programming in my brain was imposing on myself. It was completely out of my control; I felt glazed over and not with it.

As per what I’d been conditioned and instructed to do during the LP training, I told everyone that I was no longer ill and that I was recovering. I’m pretty sure that I told all my friends and family that I was in recovery, that the Lightning Process had been successful and had worked. I even had a huge 21st birthday/’I’m better now’ party in a village hall, celebrating recovery from illness. Remembering it now is upsetting. I had the biggest smile on my face the whole time and looked fine to everyone but would have to frequently escape into the toilets where I would almost black out and would collapse on the floor for a while. I was in oxygen starvation from being upright and from heart failure. I was very dizzy and everything was spinning around me because of my very low blood pressure. All my muscles were screaming at me. Nobody had any idea that this was happening to me; the LP programming prevented me from being able to tell anyone or from even acknowledging my symptoms to myself. They didn’t exist because I wasn’t ill. It’s just a haze to me now.

In the following months, I kept on pushing myself, doing insane damage to my body (I pushed myself to the point where I was going on a slow 5-minute walk every few days, which was a huge deal for me considering I had been bed-bound for two years) until one day in August 2007, when my parents were away, I pushed myself too far and went on a longer walk. At the end, my body failed and packed in completely; the six months caught up with me and I collapsed. I was never able to get up again. Ever since, I have been bed-bound, unable to sit up and unable to speak, struggling to breathe and swallow. The permanent organ damage that was done during March to August 2007 during the self-imposed GET due to the LP brainwashing, was devastating. I never recovered from it and my health has only deteriorated since. The hold that the brainwashing had over me was broken pretty quickly and thoroughly that August, thank goodness. But I can’t remember much from those six months.

Today it is being reported in the news that an experimental trial of the LP on children and teens with M.E. has been successful. The fact that the results are based on the children and teens themselves saying that they have recovered, is extremely worrying to me. During the six months that I was brainwashed with the LP, I would have said the same: that I was cured, that I was recovering and that the LP was successful. Those poor children. They are even more vulnerable than I was. What they have been subjected to is nothing short of abuse and should never have been allowed to happen in the first place.

Whatever you do, please don’t send news articles about the Lightning Process to anyone with M.E. It’s a dangerous thing. Don’t beckon lightning and invite it in for tea; it will burn your house to the ground with you inside until you’re nothing but ashes.


September 2017

The Emotional Toll Of Not Being Heard

http://www.meaction.net/2017/08/31/the-emotional-toll-of-not-being-heard/

By Christina Baltais

This story won’t be particularly unique or shocking to anyone living with ME. Every single one of us has a plethora of stories like this, and far worse than this. It has happened so many times over the last 11 years. What shocks me is the degree to which it still occurs and manages to affect me, no matter how much time I spend trying to advocate for ME.

I was out to eat with extended family members. It was my first outing in weeks, since I had been housebound due to symptoms. An outing after a long period of solitary confinement is a rather momentous occasion. I was so grateful to be out of that bed, out of that bedroom, out of that house. The vibrant world that felt so far away, I now found myself immersed in, taking in everything around me like a grateful sponge. I was basically a bear emerging from a den after a long, long hibernation (minus any refreshing sleep).

When I sat down, the usual catch-up conversation ensued. Updates on my health eventually came up. I said that its been my first outing in quite some time after a rough patch. This statement could have been followed by words that were supportive/empowering/neutral, but it wasn’t. This family member went on to comment that I looked fine, and was sitting up just fine at the table right now. I responded by saying that sitting up was actually very difficult for me because I was experiencing a great deal of weakness, and would need to rest after this outing when I got home. This was followed by a comment indicating that if I was sitting up now, why couldn’t I find a job where all I had to do was sit up and type? Why couldn’t I look for jobs like that? Was I not even going to try? After all that schooling, was I just going to waste my life?

You have got to be kidding me. (And some other words that I can’t say.)

A long uncomfortable silence ensued. I felt the familiar pangs of shame, humiliation, and judgement by someone who not only knew nothing about ME, but who also did not want to listen. No one at the table said anything in my defence, their passive silence feeling like implied agreement. I honestly believe this person’s intent was good, but how disconnected from my experience could they possibly have been to not realize the impact of their words and the implications of their statements. I really embrace the importance of talking about my body and ME as a source of education, but the first caveat always has to be that my voice and experience is heard, valued, and respected. This was another case where it clearly had not been. For if anyone was connected to the experience of ME, they would understand the absolute hell a person goes through. The depths of despair and grief this disease drags you through; it was never a choice. The inner turmoil of having a heart that wants the world everyday, but having a body constantly saying no; you forfeit any control over the direction of your life. I chose ME just as much as the millions of people around the world chose ME; we didn’t. I realize I’m preaching to the choir. The point is, I should not have to spend an outing defending and proving in hopes of understanding. I’m not wasting any precious spoons on that. It just hurts so much, still, even after 11 years.

As human beings we all need to feel love and connection. There is a deep-seated need to feel unified, to have approval, acknowledgement, acceptance—-to feel connected with, intimate and loved by, other human beings. When you are already so physically isolated due to illness, situations that make you feel emotionally and socially isolated take it to an entirely different level. It adds another layer of suffering. As if I didn’t feel disconnected and like an outsider enough already. It’s situations like this that make me realize how much during these 11 years I have not been believed or heard. It’s situations like these that make me realize how exhausting it is to constantly be vying for the understanding of others.

What’s even harder is when it comes from family, as this one did. What’s even more disheartening is that this individual is also a doctor. When I was undergoing medical training myself, some supervisors I highly respected displayed a clear lack of understanding about ME. One spoke of how you have to wonder how much of “the behaviour” is learned as it runs in families. I was told to recommend to an ME patient that they strap on a backpack full of weights and jump on a trampoline to increase bone mineral density. It was explained to me how a new physical symptom could only be psychosomatic “as anxiety is common in that demographic so that is the only plausible explanation for that extreme symptom.” Unbeknownst to them, I had ME and these comments illuminated the presumptions, assumptions, and rampant inaccuracies perpetuated by a lack of knowledge in our medical systems. They were extremely disappointing and painful to hear, as I’ve been on the receiving end of all these assumptions and exacerbating recommendations as a patient myself. The lack of knowledge and understanding is systemic; experiencing and bearing witness to how ME has been relegated to the margins of our medical system has been traumatic.

The history of ME’s constant invalidation and abhorrent lack of research funding is disturbing. I wish people would listen. I wish they would trust our experiences and accounts of our own bodies, or in some cases, of our children’s bodies. How healing the words, “I believe you,” would would be for all of us. Sometimes, the emotional toll feels worse than the actual disease itself.

We don’t know when the pathological basis of ME will finally be understood. We should not have to wait for that, to be shown the much needed empathy and compassion which we deserve. Why it takes “proof” in order to actually listen to literally millions of voices saying the same thing over decades of time baffles me. When I think of the millions of lives lived, and some ended, in complete suffering—-without voices, it enrages me. If their suffering had been validated and acknowledged, even if treatment was still not available, would it not have made a difference? The injustice of it all enrages me. Anger is often a signal something is not working, and that means something needs to change. Change is possible and can come soon for all of us. Change needs to come especially for those of us who are unable to use their voices, or even read this.

There are many ways to get involved in creating change for health equality and ME awareness. Be a part of the #TimeforUnrest global impact campaign. This campaign advocates for more recognition, education, research, and funding around ME. You can help advocate for our voices to be heard, by hosting a screening of Unrest in your community. You can join the #TimeforUnrest Facebook group, and share and promote the campaign on social media. For more ideas on how to be a part of the change, click here.

Imagine how different the world’s perception of this disease could be; and for an end to the stigma and misconceptions we’ve all experienced. Imagine with research the pathological basis of ME understood, and treatments being offered. We can make this change happen, and we can make this change happen together.

About the author: Christina, 31, lives in Toronto, ON. She holds a Bachelor’s Degree in Science and has a fine arts background. She became ill with ME while completing her Bachelors. This inspired her to become a naturopathic medical doctor in order to better understand how to heal the body. One month before completing her medical degree, her ME progressed. She has been slowly recovering, using writing, music, art, and nature as a means for processing this experience.


September 2017

At symposium, researchers and patients examine molecular basis of chronic fatigue syndrome

(Again, if only they would say ME, Myalgic Encephalomyelitis, instead of CFS)

https://www.omf.ngo/2017/08/25/community-symposium-highlights/

Posted on: August 25, 2017

by Raeka Aiyar, PhD

Ron Davis, PhD, calls chronic fatigue syndrome (also known as myalgic encephalomyelitis, or ME/CFS) the “last major disease about which we know almost nothing.” That’s because at least a million Americans are debilitated by ME/CFS, and yet no clear cause is known, no treatments are approved; funding, understanding, and awareness are disproportionately limited. Yet thanks in part to a boost in advocacy and fundraising efforts, there is increasing cause for hope, many researchers and patients believe.

Earlier this month, several hundred researchers, doctors, patients and caregivers joined forces for the Open Medicine Foundation’s Community Symposium on the Molecular Basis of ME/CFS chaired by Davis at Stanford University, with another 2,700 worldwide joining online. Known for his contributions in biotechnology and genomics, Davis has rerouted his career to tackle this disease and save his critically ill son. He’s brought together an interdisciplinary team of collaborators, many of whom spoke at the symposium. “The Human Genome Project taught us that we can take on a large project like this and succeed,” Davis said.

The event focused on a new understanding of ME/CFS as a molecular disease. Davis’ team has taken this perspective in an omics and big data study of severely ill patients. Wenzhong Xiao, PhD, Davis’ collaborator at Massachusetts General Hospital and Harvard Medical School, presented a preliminary analysis of this dataset, including efforts to use it to define biomarkers and predict causative factors.

Davis presented his technology-driven approach to unraveling ME/CFS, noting that if sequencing technologies had been available at the time, “we would have figured out AIDS in a couple of weeks.” He presented a nanotechnology developed at the Stanford Genome Technology Center that can successfully distinguish patient blood samples from healthy ones, based on their response to stress in the form of increased salt concentration. This presents the potential for a blood-based diagnostic – a transformative prospect for a field reliant on lengthy, subjective diagnoses.

A core issue in ME/CFS is massive energy depletion, so much research is focused on the mitochondria, the organelles inside cells that are responsible for energy generation. Keynote speaker and mitochondrial physiologist Robert Naviaux, MD, PhD, from the University of California, San Diego, suggested that the ‘cell danger response’ to stressors, which prevents cells from returning to baseline function until healing is complete, is prolonged in ME/CFS, which is consistent with observations of reduced metabolism in patients.

Naviaux’s theory also syncs with reports of common infections triggering the development of ME/CFS. In fact, Davis’ cell-free DNA sequencing revealed no exceptional types or levels of pathogens in patients. “It’s not the stressors themselves, but an inability to resolve them and heal afterwards,” Naviaux said.

Stanford immunologist Mark Davis, PhD, presented evidence suggesting that ME/CFS could be an autoimmune disease: using single-cell sequencing, his lab has observed an increase in patient T cells that share a particular target, a signature of an immune response. He said he is investigating what these T cells are targeting.

Nobel Laureate Mario Capecchi, PhD, from the University of Utah, presented a study in mice that shows a connection between the immune system and the brain in a genetic condition that shares some traits with ME/CFS. He also noted how important patient participation is in studying any disease, and how impressed he was with the ME/CFS patient community.

With so much patient engagement, collaboration, and community spirit – not to mention the many theories and new datasets, researchers say it is an exciting time for the field. Many attendees said they were amazed at how much has been accomplished with such scant resources. The event closed with a standing ovation.

To support ME/CFS research, please donate to OMF today. For more about the symposium, check out the YouTube video of the event or read coverage in The Mercury News.

A version of this post originally appeared on the Stanford Medicine Scope Blog.

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