Children with ME
Out of sight… Recent work looking at how to involve severely ill ME/CFS patients in research
(Taken from the Spring edition of “Breakthrough” magazine produced by ME Research UK.)
There is a considerable lack of information about those people with ME/CFS who are severely ill. They are often neglected—even though they have worse prospects of recovery—and under-represented in what little research is done.
A large part of the problem is that their challenging circumstances mean these individuals have difficulty accessing medical care and engaging in medical research. Is there any way of improving this situation?
With funding from ME Research UK, Victoria Strassheim and colleagues at Newcastle University have been conducting a programme of research concentrating on severely affected ME/CFS patients. Over the last couple of years, Victoria has published a review of existing research on severe ME, and an exploration of the effects of deconditioning in these patients. A third paper was recently published in BMJ Open, and looks specifically at how to include severely affected ME/CFS patients in research.
The first part of the project was to attempt to contact and evaluate patients with severe ME/CFS within the Northern England Clinical Network. The participants were adults with ME/CFS who were wheelchair-, house-, or bed-bound. A total of 483 questionnaire packs—including the Barthel Functional Outcome Measure and the De Paul fatigue questionnaire—were sent out to those people identified.
Unfortunately, only 63 packs were returned, although 76% to 88% of participants managed to complete the questionnaires successfully. The responses provided a host of information on the burden of symptoms and functional difficulties patients have to live with. The findings of the survey are freely available to download from the BMJ Open website: bit.ly/StrassheimSurvey.
The second part of the project involved making a series of home visits to five severely ill ME/CFS patients, and attempting to complete assessments previously conducted in people with mild or moderate ME/CFS.
Over the course of four visits, a number of activities were attempted, including various physical and respiratory tests, cognitive assessments, and several questionnaires. Two patients were able to complete all of the assessments, while the other three achieved around 50%, and were unable or refused to perform the other tests, or could not attend due to ill health.
The investigators conclude that people severely affected by ME/CFS can engage with research, but they have a considerable burden of symptoms and a poor quality of life, and they need more support during the research process. The use of “research advocates” is suggested, to help engage and recruit these individuals into clinical studies.
He pioneered technology that fueled the Human Genome Project. Now his greatest challenge is curing his own son
By Ryan Prior, CNN
May 12, 2019
(CNN) – Multiple times a day, every day, Ron Davis sits with his head bowed, waiting outside his son’s bedroom for a subtle signal that it’s all right to come in.
He opens the door to the space where Whitney has spent most of the last decade.
Whitney lies motionless on a simple bed, his head shaved and his frame emaciated. He’s fed by a tube directly into his stomach. His lips haven’t uttered a word in five years.
Davis, who is 77, leads a lab that invented much of the technology that powered the Human Genome Project. Now he and his wife spend much of their days caring for their 35-year-old son, who is immobilized by myalgic encephalomyelitis, or chronic fatigue syndrome (ME/CFS).
Sunday is ME/CFS International Awareness Day. There is no cure. But Davis is leading a global push to root out the molecular basis of what is laying waste to Whitney and millions of other sufferers around the world so that scientists can better treat the disease.
Davis signals to his wife, Janet Dafoe, that Whitney is ready. She goes in and wipes her son’s face. She pulls the covers up toward his head while he lies motionless.
She fixes an IV bag to a pole, which will drip water into her son’s veins.
Davis sinks to his knees and takes Whitney’s socks off. He clips his son’s toenails. He washes his son’s feet.
For the couple, it’s a holy moment.
Davis led a revolution in science
Davis and Dafoe will celebrate their 50th wedding anniversary in July. Decades ago, they would have never predicted their current situation.
Now their everyday lives are consumed with caring for their son. At least one of them must be at home every day to attend to Whitney.
“My wife and I can’t go away together anymore,” Davis says. They used to go to the beach every year, but it’s been more than seven years since they last went. On basically a single income, they struggle with finances.
“It has turned my life upside down in many respects. I decided to terminate everything I was working on before Whitney got sick,” Davis says. “Everything is ME/CFS now. It’s an emergency kind of effort.”
The couple have spent their careers in and around Stanford University. Davis worked for decades in the school’s biochemistry and genetics department while Dafoe, who just turned 70, works as a child psychologist. She has scaled back her hours to about five hours a week to care for her son.
After his PhD at Caltech, Davis completed his postdoc at Harvard studying under Nobel Laureate Jim Watson of “Watson and Crick” fame, who was immortalized in science textbooks for co-discovering the double-helix structure of DNA in 1953.
Davis joined Stanford’s biochemistry department in 1972 as an associate professor and quickly began making a name for himself.
He co-wrote one paper that created a map with a new way to link genes to the traits they caused, which became a cornerstone of the field of genomics. It led Davis and his colleague to write a “proposal for a map of the whole human genome.” The National Institutes of Health turned them down in 1979, saying their plan was too ambitious.
But Davis kept innovating, eventually accumulating more than 30 patents for technology he developed.
Finally, the world caught up to his vision. The $3.8 billion Human Genome Project began in 1990, with Davis’ gene-sequencing technologies at its core. Completed in 2003, it launched a revolution in science. Handing researchers that foundational blueprint for human life gave biologists and doctors what up to that point was an unimagined power to diagnose, treat and ultimately prevent the full gamut of human disease.
Davis was shortlisted by The Atlantic, along with SpaceX founder Elon Musk and Amazon founder Jeff Bezos, as someone tomorrow’s historians will consider today’s greatest inventors.
The same prescient mind that dreamed up the Human Genome Project now devotes days to what Davis calls “the last great disease to conquer.”
He may need all his brilliance to save his son.
But then his son got sick, and his priorities changed
Davis and Dafoe raised their two children in a quiet Palo Alto neighborhood. Each year they backpacked as a family in California’s Sierra mountains, disappearing for weeks at a time.
“I carried Whitney up there when he was young,” Davis says. On one of these trips 5-year-old Whitney impressed his father by walking nine miles in a single day. On another Sierras trip their baby daughter Ashley took her first steps at 5,000 feet above sea level.
“I haven’t gone in 10 years now,” Davis says. “I would love to do that with Whitney again.”
By 2008, Whitney, was 24 and living in a small town in Nevada, knocking on doors for then-Sen. Barack Obama’s presidential campaign.
But he often complained about being exhausted. A skilled photographer, Whitney captured images at Obama’s inauguration in 2009, but even then he could no longer work a full day.
After years of declining health, seeing numerous doctors and not getting answers, Whitney was finally diagnosed with ME/CFS.
As his health worsened, he moved in with his parents in May 2011. He tried to keep working as a wedding photographer but soon gave that up because he needed a week to recover from shooting a single wedding. He soon became mostly bedridden.
In his last post on his photography website, Whitney lamented that “chronic fatigue syndrome” couldn’t do justice to his condition. He preferred “total body shutdown.”
Whitney has lost the ability to speak — something a very small fraction of ME/CFS patients experience. Dafoe says he used to communicate with the family via text messages, but that skill is now lost too, as even the glow of a smartphone screen is too much stimulation for him. The heart emojis he sent to his caregivers are just memories now.
Eventually he could no longer eat solid food.
In one of his last texts to his parents, he wrote, “I’m sorry I’m ruining your golden years.”
To seek a cure, Davis recruited a dream team of researchers
Over a life spent at the frontiers of science, Davis has collaborated with many accomplished researchers. He’s cashing in on those relationships now in building a world-class team he hopes can find the molecular basis for ME/CFS.
“I made phone calls, and everybody I called said yes,” Davis says.
Some of his colleagues had never heard of the disease. He told them it affected 1% of the population, or about one in 300 Americans. He told them the National Institutes of Health at the time was dedicating less than $6 million annually to researching the disorder.
That poses a challenge in tackling an illness that lacks an FDA-approved treatment, doesn’t have a known cause or a singular lab test for clinicians to diagnose it. ME/CFS has lagged behind in the bio-medical imagination compared with cousins like multiple sclerosis, which also affects the immune system and the nervous system.
Following outbreaks in the 1980s, some dismissively called chronic fatigue syndrome the “yuppie flu.”
But its symptoms, which include constant exhaustion, pain, brain fog and unrefreshing sleep, can be as disabling as late-stage cancer. Taking a shower may leave someone with ME/CFS bed-bound and unable to do anything for days.
In 2017, NIH doubled its research spending on the disease to $12 million. But Davis argues that compared to other diseases of similar severity and prevalence, that’s not nearly enough. Multiple sclerosis, a disease that affects fewer patients than ME/CFS, attracts more than $100 million a year in NIH-funded research.
Davis now regularly convenes top scientists via an advisory board he set up through the Open Medicine Foundation, a California-based non-profit that’s raised $18 million to research the disease. Its hub is Davis’ Stanford Genome Technology Center, making Davis unique among living scientists in his ability to coordinate the discovery of a cure.
But to make the kind of progress he and his colleagues envision, they need a lot more money.
They are making slow but steady progress
ME/CFS patients, like those with multiple sclerosis and other diseases, fall on a spectrum. Some are still able to go to an office and work, while others are bedridden 23 or more hours a day.
At research conferences, Davis sometimes sits and talks with ME/CFS patients for hours.
“I’m very sympathetic to them,” he says. “It makes me feel that I have to solve this, but not in an arrogant way. I just know I have to put every ounce of energy into this to help all the patients, which also include my son.”
Davis and Dafoe know there’s a vibrant mind and spirit alive in their son’s weakened body. Whitney is a devout Buddhist, and their house is strewn with prayer flags. Dafoe thinks Whitney spends much of his day meditating.
When Whitney’s younger sister Ashley got married, Dafoe pointed to the ring on her finger to pantomime the happy news to her son. The two siblings had been very close. Whitney didn’t speak, but held his hands to his heart and wept with joy.
At Davis’ lab, Whitney’s blood samples are among many churning away in sequencing machines, contributing to what his organization believes is the deepest study of ME/CFS patients ever attempted.
This wouldn’t be the first time Davis has set his sights on a problem the scientific establishment found unsolvable. “You have to look for those,” he says.
He and his team have been hard at work the past few years. One of their inventions, a “nanoneedle” for testing blood, speaks to the need to find a single biomarker in patients’ blood.
A blood test which identifies a specific molecular abnormality unique to ME/CFS patients has long been a sticking point in researchers’ quest to get the disease more recognized. Having one could spur more drug development, because pharmaceutical companies would understand the root of what’s wrong with patients.
Davis’ team has tested their nanoneedle with initial success and recently published their findings in a scholarly journal. They discovered ME/CFS patients’ blood responds to the introduction of “stress” — in this case, salt — differently than the blood of healthy people. Davis hopes the device will ultimately produce a cheap clinical test by which doctors can identify ME/CFS quickly and accurately.
He also wants to explore measures to prevent the disease. For example, he wants to understand why people with mononucleosis often develop ME/CFS.
Those are just a few of many things Davis’ team are working on.
“We don’t have enough money, so we have to prioritize,” he says.
Davis flew to Washington in early April for a symposium about ME/CFS. He almost didn’t make the trip because it would leave his wife at home alone, caring for Whitney while she had the flu.
But she told him he had to go.
Caring for Whitney is a daily ritual
Davis and Dafoe sometimes wait for hours outside Whitney’s room, peering through a keyhole to see whether he has assumed a position in bed indicating it’s all right to come in. With words no longer an option, they must interpret Whitney’s postures and occasional hand signals.
Six times each day, every day, they perform this ritual, silently, dutifully, shut off from the gaze of the world.
They start around 2:30 p.m., first hooking up Whitney’s IV. On the next entry into his room, they hook up the pump for the “j-tube” that will send nutrients directly into their son’s stomach.
On the third visit, they wash and clean the small plastic vessels next to Whitney’s bed that he uses as urinals. Next they come back in to put the urinals on Whitney’s stomach for when he’s ready to use them again. On their last visit, often around 2:30 a.m., they’ll put ice on Whitney’s stomach to help soothe his excruciating digestive pains.
“I feel like I’m living in a different world. It’s hard to say anything when people ask ‘how are you doing?'” Dafoe says. “Our world has just been consumed by a chronic illness.”
There’s a disciplined intentionality behind their movements. For Whitney, the tiniest deviation in their procedure can be devastating.
“His cognitive processes don’t work right,” Dafoe says. She and her husband wear plain shirts with no lettering when they’re in Whitney’s room because the sliver of energy it takes his brain to process a word can cause him to crash. They even use tape to cover labels on tubes of Neosporin.
Such crashes cause Whitney severe stomach pain, which make it impossible for them to put more food in his feeding tube.
Dafoe wants her husband to get enough sleep so that he can stay fresh and focused on researching the disease. That means on many nights she’s up until 5 or 6 a.m. helping Whitney.
By 5 p.m. she’s back to caring for her son.
They hope their son’s suffering can have a greater purpose
“I got a PhD. That was hard,” Dafoe says. “I’ve climbed mountains. That was hard.”
But she says enduring Whitney’s illness is the most difficult thing she’s done in her life, “by a factor of thousands.”
One simple truth guides her. “He’s my son. I just love him.”
Dafoe receives messages from ME/CFS patients all over the world who say they are inspired by her husband and alarmed by her son’s severe condition. She says she feels like a mother to these people, many of whom are suicidal — a rational response to a life spent hovering just above death.
Many tell her Whitney is their north star. They say if he can go on living through hell, year after year, then their suffering must be endurable too.
“He’s saving lives,” Dafoe says. “Just by lying there.”
Nearly all her and her husband’s communication with Whitney is through pantomimed gestures. If he wants more of something he’ll hold his hands together, then bring them apart.
But every so often the fog lifts a little and Davis and Dafoe can speak more complex ideas aloud to Whitney. A few months ago, they told him how prominent his father has become in the field of scientists researching his disease.
“He was really excited about that,” Dafoe says.
Whitney punched the air like a boxer, signaling that he intends to fight on.
Ryan Prior is a cross-platform associate producer at CNN. He was diagnosed with chronic fatigue syndrome in 2007 and wrote about that experience here.
CBT for ME/CFS is not effective
Cognitive behavioural therapy for myalgic encephalomyelitis/chronic fatigue syndrome is not effective. Re-analysis of a Cochrane review
Mark Vink, Alexandra Vink-Niese
First Published May 2, 2019
Analysis of the 2008 Cochrane review of cognitive behavioural therapy for chronic fatigue syndrome shows that seven patients with mild chronic fatigue syndrome need to be treated for one to report a small, short-lived subjective improvement of fatigue. This is not matched by an objective improvement of physical fitness or employment and illness benefit status. Most studies in the Cochrane review failed to report on safety or adverse reactions. Patient evidence suggests adverse outcomes in 20 per cent of cases. If a trial of a drug or surgical procedure uncovered a similar high rate, it would be unlikely to be accepted as safe. It is time to downgrade cognitive behavioural therapy to an adjunct support-level therapy, rather than a treatment for chronic fatigue syndrome.
For years, the recommended treatments for chronic fatigue syndrome (CFS) have been cognitive behavioural therapy (CBT) and graded exercise therapy (GET). These recommendations have been based on Cochrane reviews (Larun et al., 2017; Price et al., 2008) and a large randomised controlled trial by White et al. (2011), informally referred to as the PACE trial (‘Pacing, graded Activity, and Cognitive behaviour therapy; a randomised Evaluation’). This trial concluded that CBT and GET were moderately effective treatments, leading to recovery in 22 per cent of patients. Due to its size (n = 640) and promotion, it has been very influential in the promotion of CBT and GET as effective treatments for CFS (Wilshire et al., 2018b). Recently, a number of re-analyses of the PACE trial, including a special issue of the Journal of Health Psychology (Marks, 2017), have raised significant concerns with the published outcomes of the trial. If the PACE trial had not made a significant number of outcome changes, which led to an overlap in entry and recovery criteria, then there would not have been a difference in recovery rate between CBT and GET and the two control groups (no treatment (specialist medical care) and adaptive pacing therapy) (Geraghty, 2017a; Vink, 2016; Wilshire et al., 2018b). Essentially, the recovery rate would have been the same as the natural occurring one (Cairns and Hotopf, 2005). The absence of objective improvement in the PACE trial (fitness and 6-minute walk test (6MWT)) and the increase in illness and unemployment benefits, matched the findings from the evaluation of the use of CBT and GET in the Belgium CFS knowledge centres (Stordeur et al., 2008). As noted by O’Leary (2018), ‘although PACE [has] dictated management of ME/CFS across the globe for many years, the study fails to meet basic standards of scientific methodology’. ‘Indeed, it is difficult to imagine how such a large-scale investigation could have developed, proceeded and passed through the review process unless its scientific failings were actually characteristic of its field’. Analysis of the Dutch FITNET trial of Internet CBT for adolescents (Ghatineh and Vink, 2017), of the Dutch FatiGo trial of multidisciplinary rehabilitation treatment (Vink and Vink-Niese, 2018a) and of five Dutch hallmark CBT studies (Twisk and Corsius, 2017) supported this observation. A recent re-analysis of the Cochrane exercise review for CFS (Vink and Vink-Niese, 2018b) revealed a number of methodological concerns with many of the studies reviewed as part of the Cochrane review of GET for CFS and a lack of objective evidence for improvement in physical function. It also showed that the problems noted by O’Leary are not confined to Dutch studies. O’Leary also concluded that ‘the PACE controversy suggests a need to evaluate the scientific credibility of psychosomatic medicine generally’. As such, we carried out an analysis of the Cochrane review of CBT treatment for CFS by Price et al. (2008), to ascertain if this review contained any of the problems identified in Vink and Vink-Niese (2018b), by O’Leary (2018) or Geraghty (2017a) and also to assess whether or not the conclusions of this Cochrane review – that CBT is somewhat effective with moderate size effects – is justified by the data contained within the primary studies included in the review. In our analysis, we concentrated on the objective outcome measures to establish if improvements in self-report (fatigue) translate to observable improvement in objective tests (physical ability, fitness, etc.) as there is an inverse relationship between fatigue and physical activity (Rongen-van Dartel et al., 2014).
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Something in the blood
Remarkably, four independent groups have now found evidence that a factor in the blood can affect cell metabolism/mitochondria in ME/CFS and transfer the effect to healthy cells. Here is a summary of the provisional findings.
The first to find the effect were Dr Oystein Fluge and Professor Olav Mella in 2016.
They were studying energy production in the cell, a logical thing to do when trying to understand an illness where energy is in such short supply.
Cells have two ways to convert food molecules into usable energy. Glycolysis is a process in the cell cytoplasm that extracts a small amount of energy from carbohydrate molecules, producing lactate. But the real houses of energy production are mitochondria, which burn up food molecules with oxygen, producing large amounts of usable fuel.
Fluge and Mella used an expensive bit of kit called the Seahorse analyser, which measures glycolysis through the lactate production and mitochondrial activity through changes in oxygen levels.
They tested normal healthy muscle cells that had been grown in the lab. But they added to those cells serum taken from either ME/CFS patients or healthy controls. Serum is the fluid left over after blood has clotted and it contains small molecules and other soluble substances.
They have data for 12 people with ME/CFS and 12 healthy controls, a relatively small sample.
What they found was, surprisingly, that the muscle cells produced more lactate and burned more oxygen when they were incubated with ME/CFS serum than when incubated in serum from healthy controls. And the effect was particularly strong when the cells were made to work hard.
So something in the serum (which comes from blood) of ME/CFS patients is affecting healthy cells, and somehow making them work harder.
This is the only published study to date, but three other groups have revealed related findings at conferences.
Dr Ron Davis provided the most dramatic demonstration of the effect in a plasma swap experiment using his nanoneedle test. Plasma is the liquid left over when solid matter has been removed from blood: the the red and white blood cells, and platelets.
The nanoneedle chip measures electrical impedance of cells. In the presence of salt (which stresses the cells because they have to use energy to pump the salt out) the impedance of cells in ME/CFS blood increases much more than cells in blood taken from healthy controls.
Davis’s group then ran an elegant experiment using this set up. They put blood cells from healthy donors in plasma from ME/CFS patients and found that the healthy cells behaved like ME/CFS ones did, with a big increase in electrical impedance. And when they put ME/CFS cells in plasma from healthy controls, they found that these ME/CFS cells behave like healthy cells.
So plasma from ME/CFS patients makes healthy cells behave like ME/CFS ones. And plasma from healthy controls makes ME/CFS cells behave like healthy ones. These are stunning findings.
We don’t know the sample size for this study but hopefully more details will be available soon as a paper has been accepted for publication in the Journal PNAS.
Karl Morten, Oxford university
Like Fluge and Mella, Dr Karl Morten looked at mitochondria/energy metabolism in lab grown muscle cells and also saw an effect.
His group used a molecular probe to measure oxygen concentration within cells to track the activity of mitochondria.
They found that adding plasma from healthy controls made no difference to oxygen levels of the muscle cells. But adding plasma from ME/CFS patients caused oxygen levels to fall, indicating that the mitochondria were working harder (a similar result to Fluge and Mella).
Morton said he didn’t know why the mitochondria were working harder: he said it might be that they were working less efficiently, but the goal was to find out.
The study used over 30 patients and Morton noted that on average the levels were lower for patients than for controls. He suggested this might be due to a subgroup effect, where only some patients had the effect, with around a third of patients scoring below the lowest oxygen level for healthy controls.
Bhupesh Prusty, Wuerzburg university
Dr Bhupesh Prusty has also looked at the effect of a blood factor on mitochondria, but his work focuses on a less well-known role of mitochondria, in immunity against viruses.
Although mitochondria are normally shown as single bacteria- or bean-like units, the reality is more complex. In living cells, mitochondria constantly fuse together and separate, and the fact that they are often fused together, like a string of beans, is important for their ability to fight viruses.
Some viruses, including HHV-6, fight back by causing mitochondria to fragment back into their single forms, reducing their ability to fight viruses.
Serum from ME/CFS patients causes mitochondria that were fused together to fragment, whereas plasma from healthy controls does not.
So far, the group have only looked at five patients and three controls, so these are very provisional results.
In a separate experiment, his group showed that the effect was reversible (they washed away patient serum after three days and mitochondria gradually resumed normal fusing behaviour).
Fluge’s and Morten’s studies are directly linked to energy metabolism. Davis’s is indirectly: the salt added to the nanoneedle test forces the cell to use energy pumping sodium out of the cell. The Prusty research looks at mitochondria, but the changes in morphology are apparently linked to cell defence rather than to energy production.
At the recent NIH conference, Ron Davis said that their work indicates that the factor in the blood responsible for all this are exosomes, tiny membrane-bound packets of biomolecules released by cells. Exosomes are a type of extracellular vesicle, and these are taken up by cells and are believed to be involved in cell to cell communication, though their role is as yet unclear. Extracellular vesicles are being studied by Dr Maureen Hanson as part of her collaborative’s work.
So we have four groups finding that a factor in ME/CFS blood that has an effect on cells. These are still early days: only one study has been published so far, the sample sizes are relatively small and the findings need to be confirmed. But if things pan out, this development could prove to be an important step in understanding the biology of at least some types of ME/CFS.
Press Release: Biomarker for chronic fatigue syndrome identified
April 29, 2019
Stanford scientists devised a blood-based test that accurately identified people with chronic fatigue syndrome, a new study reports.
People suffering from a debilitating and often discounted disease known as chronic fatigue syndrome may soon have something they’ve been seeking for decades: scientific proof of their ailment.
Researchers at the Stanford University School of Medicine have created a blood test that can flag the disease, which currently lacks a standard, reliable diagnostic test.
“Too often, this disease is categorized as imaginary,” said Ron Davis, PhD, professor of biochemistry and of genetics. When individuals with chronic fatigue syndrome seek help from a doctor, they may undergo a series of tests that check liver, kidney and heart function, as well as blood and immune cell counts, Davis said. “All these different tests would normally guide the doctor toward one illness or another, but for chronic fatigue syndrome patients, the results all come back normal,” he said.
The problem, he said, is that they’re not looking deep enough. Now, Davis; Rahim Esfandyarpour, PhD, a former Stanford research associate; and their colleagues have devised a blood-based test that successfully identified participants in a study with chronic fatigue syndrome. The test, which is still in a pilot phase, is based on how a person’s immune cells respond to stress. With blood samples from 40 people — 20 with chronic fatigue syndrome and 20 without — the test yielded precise results, accurately flagging all chronic fatigue syndrome patients and none of the healthy individuals.
The diagnostic platform could even help identify possible drugs to treat chronic fatigue syndrome. By exposing the participants’ blood samples to drug candidates and rerunning the diagnostic test, the scientists could potentially see whether the drug improved the immune cells’ response. Already, the team is using the platform to screen for potential drugs they hope can help people with chronic fatigue syndrome down the line.
A paper describing the research findings was published online April 29 in the Proceedings of the National Academy of Sciences. Davis is the senior author. Esfandyarpour, who is now on the faculty of the University of California-Irvine, is the lead author.
Providing the proof
The diagnosis of chronic fatigue syndrome, when it actually is diagnosed, is based on symptoms — exhaustion, sensitivity to light and unexplained pain, among other things — and it comes only after other disease possibilities have been eliminated. It is also known as myalgic encephalomyelitis and designated by the acronym ME/CFS. It’s estimated that 2 million people in the United States have chronic fatigue syndrome, but that’s a rough guess, Davis said, and it’s likely much higher.
For Davis, the quest to find scientific evidence of the malady is personal. It comes from a desire to help his son, who has suffered from ME/CFS for about a decade. In fact, it was a biological clue that Davis first spotted in his son that led him and Esfandyarpour to develop the new diagnostic tool.
The approach, of which Esfandyarpour led the development, employs a “nanoelectronic assay,” which is a test that measures changes in miniscule amounts of energy as a proxy for the health of immune cells and blood plasma. The diagnostic technology contains thousands of electrodes that create an electrical current, as well as chambers to hold simplified blood samples composed of immune cells and plasma. Inside the chambers, the immune cells and plasma interfere with the current, changing its flow from one end to another. The change in electrical activity is directly correlated with the health of the sample.
The idea is to stress the samples from both healthy and ill patients using salt, and then compare how each sample affects the flow of the electrical current. Changes in the current indicate changes in the cell: the bigger the change in current, the bigger the change on a cellular level. A big change is not a good thing; it’s a sign that the cells and plasma are flailing under stress and incapable of processing it properly. All of the blood samples from ME/CFS patients created a clear spike in the test, whereas those from healthy controls returned data that was on a relatively even keel.
“We don’t know exactly why the cells and plasma are acting this way, or even what they’re doing,” Davis said. “But there is scientific evidence that this disease is not a fabrication of a patient’s mind. We clearly see a difference in the way healthy and chronic fatigue syndrome immune cells process stress.” Now, Esfandyarpour and Davis are expanding their work to confirm the findings in a larger cohort of participants. Recruitment for the larger project, which aims to further confirm the success of the diagnostic test, is being done on a rolling basis. Those who are interested in participating should contact clinical research coordinator Anna Okumu.
In addition to diagnosing ME/CFS, the researchers are also harnessing the platform to screen for drug-based treatments, since currently the options are slim. “Using the nanoelectronics assay, we can add controlled doses of many different potentially therapeutic drugs to the patient’s blood samples and run the diagnostic test again,” Esfandyarpour said.
If the blood samples taken from those with ME/CFS still respond poorly to stress and generate a spike in electrical current, then the drug likely didn’t work. If, however, a drug seems to mitigate the jump in electrical activity, that could mean it is helping the immune cells and plasma better process stress. So far, the team has already found a candidate drug that seems to restore healthy function to immune cells and plasma when tested in the assay. The drug, while successful in the assay, is not currently being used in people with ME/CFS, but Davis and Esfandyarpour are hopeful that they can test their finding in a clinical trial in the future.
All of the drugs being tested are either already approved by the Food and Drug Administration or will soon be broadly accessible to the public, which is key to fast access and dissemination should any of these compounds pan out.
Davis is a member of Stanford Bio-X, the Stanford Cancer Institute and the Stanford Maternal & Child Health Research Institute.
Other Stanford authors of the study are research scientists Neda Nemat-Gorgani and Julie Wilhelmy and research assistant, Alex Kashi.
The study was funded by the Open Medicine Foundation. Davis is the director of the foundation’s scientific advisory board.
ME Association: Forward ME and Oxford Brookes University Announce Results of Patient Survey on CBT and GET in ME/CFS | 03 April 2019
We are pleased to be able to let you see the results of the recent survey conducted on behalf of Forward-ME.
All the raw data was analysed and inserted into a comprehensive report by Professor Helen Dawes and Her team at Oxford Brookes University.
“The results show clearly that cognitive behavioural therapy and graded exercise therapy are unsuitable treatments or management approaches for ME/CFS. The changes in severity and the worsening of symptoms are clear indications that the therapies being offered are having adverse effects on the health of individuals.”
Forward ME, Executive Summary, April 2019.
Bearing in mind that this survey was organised at very short notice and that we are aware that there are some shortcomings – such as a selective bias in that only people with on-line access and the ability to complete the questionnaire were included – we are very grateful to all who responded so quickly.
The results have been well received by the Chairman of the NICE Guideline Development Group and will, we hope, be helpful to the Group as they develop the new guideline for ME/CFS.
NICE Patient Survey Outcomes CBT and GET: Forward ME Executive Summary (reproduced below).
NICE Patient Survey Outcomes CBT and GET: Full report: Evaluation of a survey exploring the experiences of adults and children with ME/CFS who have participated in CBT and GET interventional programmes (Published, 03 April 2019)
Latest Minutes: Forward ME with Professor Helen Dawes from Oxford Brookes University, 13 March 2019 (Published, 03 April 2019)
Evaluation of a survey exploring the experiences of adults and children with ME/CFS who have participated in CBT and GET interventional programmes
Executive Summary from Forward ME
This survey was commissioned by Forward ME following discussions between the Chair and Vice-Chair of the NICE Guideline Development Group, Members of Parliament and the Chair of Forward-ME about the lack of up-to-date data about providing additional patient evidence relating to long-term outcomes and harms following Cognitive Behavioural Therapy (CBT) and Graded Exercise Therapy (GET).
The survey was designed by a steering group of Forward ME members and an independent research unit within Oxford Brookes University, Oxford Clinical Allied Technology and Trials Services Unit (OxCATTS), was engaged to undertake the survey, collate, analyse and report on the response.
Due to the short timescales involved, the survey was only available online and it was not possible to allow paper responses. Please note, this will mean that a number of people with ME, particularly those who are severely affected, will not have been able to have their experiences considered.
The survey was designed to gather evidence from people who have been offered CBT and/or GET based on the current NICE Guidelines since 2007. Much of the evidence received echoes what we already know from previous surveys and feedback received by charities over a number of years.
The full report follows this executive summary. We set out below the key findings that we have drawn from it. We acknowledge that there may be some bias in the results of the survey due to its promotion by ME charities rather than NHS organisations.
There are also limitations in self-reported data however we feel the scale of the response demonstrates the strength of feeling and harm on the issue.
2,274 survey responses were received. Of these, 80.4% identified as female and 16.0% as male, with the remaining choosing ‘non-binary’ or ‘prefer not to say’.
98.5% said they experience post-exertional malaise. This is shown in the chart opposite.
8% were aged 18 or under and the age band with the highest responses rate was 41-50 at 26.6%.
Cognitive Behavioural Therapy (CBT)
789 people said they were offered a course of CBT with 84.9% starting the course.
We asked whether any symptoms worsened because of the treatment. 46.6% said yes and 48.5% said no. The most common symptoms mentioned were fatigue and pain. 21.6% also developed new symptoms.
We asked people ‘‘what severity is their condition both before and after treatment?’. The percentage of people describing their condition as severe before treatment was 10.9% and this increased to 19.1% after treatment. Of those who started the course, we asked ‘what impact did CBT have on their physical and mental health?’. See results in chart.
“CBT, while may be effective for a minority in helping with mental health challenges such as depression or anxiety, is shown to be ineffective in a considerable proportion of people and even led to almost half of respondents reporting worse symptoms.”
Forward ME, Executive Summary, April 2019.
Graded Exercise Therapy (GET)
542 people said they were offered a course of GET with 79% starting the course.
We asked whether any symptoms worsened because of the treatment. 81.1% said yes and 13.3% said no. The most common symptoms mentioned were fatigue and pain. 36.7% also developed new symptoms.
We asked people ‘‘what severity is their condition both before and after treatment?’. The percentage of people describing their condition as severe before treatment was 12.9% and this increased to 35.3% after treatment.
Of those who started the course, we asked ‘what impact did GET have on their physical and mental health?’. See results in chart.
“GET is shown to cause considerable deterioration in physical and mental health. It has led to people becoming more severe and the open questions have given us insight into the worsening symptoms that have developed when patients have increased their activity beyond their capabilities.”
Forward ME, Executive Summary, April 2019.
CBT with GET combined
943 people said they were offered a course of CBT with GET combined with 76.9% starting the course.
We asked whether any symptoms worsened because of the treatment. 58.3% said yes and 37.7% said no. The most common symptoms mentioned were fatigue and pain. 29% also developed new symptoms.
We asked people ‘‘what severity is their condition both before and after treatment?’. The percentage of people describing their condition as severe before treatment was 12.6% and this increased to 26.6% after treatment.
Of those who started the course, we asked ‘what impact did CBT with GET combined have on their physical and mental health?’. See results in chart.
GET combined with CBT
943 people said they were offered a course of GET with CBT with 75% starting the course.
We asked whether any symptoms worsened because of the treatment. 85.9% said yes and 10.3% said no. The most common symptoms mentioned were fatigue and pain. 44.4% also developed new symptoms.
We asked people ‘‘what severity is their condition both before and after treatment?’. The percentage of people describing their condition as severe before treatment was 13.2% and this increased to 41.9% after treatment.
Of those who started the course, we asked ‘what impact did GET combined with CBT have on their physical and mental health?’. See results in chart.
The results show clearly that cognitive behavioural therapy and graded exercise therapy are unsuitable treatments or management approaches for ME/CFS. The changes in severity and the worsening of symptoms are clear indications that the therapies being offered are having adverse effects on the health of individuals.
CBT, while may be effective for a minority in helping with mental health challenges such as depression or anxiety, is shown to be ineffective in a considerable proportion of people and even led to almost half of respondents reporting worse symptoms.
GET is shown to cause considerable deterioration in physical and mental health. It has led to people becoming more severe and the open questions have given us insight into the worsening symptoms that have developed when patients have increased their activity beyond their capabilities.
The results show that although NICE might not recommend GET for the severely affected, they are clearly being given GET at the clinical level. This could be because clinics are not tailoring their management advice to the individual (as NICE recommends) or are simply not aware of the unsuitability of aerobic/exercise for people with ME/CFS.
Alongside this the analysis of the survey provided by Oxford Brookes University show that people with ME/CFS have experienced negative effects with regard to welfare and benefits when choosing whether or not participate in these treatments. Results also show that the adverse effects of the treatment has had a considerable impact on the employment and education capabilities of individuals.
We acknowledge that there may be some bias in the results of the survey due to the promotion of the survey being organised by ME charities rather than NHS organisations. There are also limitations in self-reported data. However, we feel the scale of the response demonstrates the strength of feeling and harm on this issue.
As there is a commitment that this new guideline be ‘patient led’ we believe that the responses should carry considerable weight in the consideration of effective treatment or management approaches. There is also an ethical question whether the current management recommendations relating to CBT and GET can continue while the development is underway when their suitability is evident.
Our collective recommendation is that GET and CBT be removed from the NICE guideline for ME/CFS.
Information about Forward ME
Forward-ME consists of a fairly broad spectrum of charities and voluntary organisations invited by the Countess of Mar to meet from time to time. The Aim of Forward-ME is to promote effective joint working by ME and CFS organisations to maximise impact on behalf of all people with ME and CFS in the UK.
Forward-ME has no formal constitution. It exists to improve recognition, understanding, research, management, support and information for everyone whose life is affected by ME and CFS.
The linked organisations and associates are:
Countess of Mar (Chair), Carol Monaghan MP (vice chair), Dr Nigel Speight, Dr William Weir, Dr Nina Muirhead, ME Association, ME Research UK, Action for ME, TYMES Trust, reMEmberCFS, BRAME, ME Trust, BRAME, 25% ME Group, #MEAction.
MEA Summary Review: Assessing PEM – The characteristic symptom of ME/CFS
Charlotte Stephens, Research Correspondent, ME Association.
Post-exertional malaise (commonly referred to as PEM) is considered a hallmark characteristic of ME/CFS. However, it is not a requirement in many of the different diagnostic criteria.
There is currently no agreed upon definition of PEM, nor a formal assessment for its measurement, but creating one could improve future diagnosis of the disease.
Dr Melvin Ramsay – the clinical champion of M.E. and founding member of the ME Association – originally described what has since become known as PEM, as:
“Muscle fatigability whereby, even after a minor degree of physical effort, three, four, or five days, or longer, elapse before full muscle power is restored and constitutes the sheet anchor of diagnosis.”
“Without it I would be unwilling to diagnosis a patient as suffering from ME, but it is most important the stress the fact that cases of ME of mild or even moderate severity may have normal muscle power in remission.”
The Saga of the Royal Free Disease (50th Anniversary Reprint).
Since then the definition of PEM has expanded, but no single version or means of assessment has really prevailed (see References for recent research on this topic).
However, in recent years we have witnessed the development of objective evidence that supports PEM as a real and unique symptom.
Earlier this month Professor Lenny Jason and his team from the Center for Community Research at DePaul University in Chicago, published results of a large public survey on PEM.
They hope the analysis will lead to a definitive definition and will ultimately provide a validated clinical assessment tool.
In this review, we hope to explain what PEM is, cover some of the research surrounding it and give an overview of the results from this latest research.
Looking back with ME on Amazon Kindle
I am pleased to say that my little book “Looking back with ME” is now available as an Amazon kindle book – click here. (It is available on the Kindle Unlimited scheme, for anyone who subscribes to it.) Many people with ME (myself included) find it easier to read books on a kindle rather than the printed variety, so I am hoping that having the book for Amazon kindle might be a help to some. (Just in case anyone is wondering, I don’t make any money from either the printed or e-book versions.)
Chronic Fatigue Syndrome: It’s Real, and We Can Do Better
My name is Dr Elizabeth Unger and I am chief of CDC’s Chronic Viral Diseases Branch, which houses the myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) program.
An estimated 836,000 to 2.5 million Americans suffer from ME/CFS, a serious, long-term illness that can severely impair the ability of those affected to live normal lives. But the majority of those affected are not diagnosed, and many struggle with symptoms for years before receiving a diagnosis.
The absence of a definitive diagnostic test contributes to this problem. In addition, most medical schools in the United States do not include ME/CFS in their physician training.
Less than one third of medical school curricula and less than half of medical textbooks in the United States address ME/CFS, so many healthcare providers need more information about this condition.
When I meet with those living with ME/CFS and their loved ones, the overarching concern that I hear is the difficulty finding good healthcare from informed and compassionate providers.
To address this need, we released an updated CDC website about ME/CFS for healthcare providers in July 2018. The new site was designed specifically with clinicians in mind. It offers information about how clinicians can better assess and help their patients manage this illness.
The new content includes:
- Presentation and clinical course of ME/CFS;
Prognosis, epidemiology, and possible causes of ME/CFS;
Diagnostic criteria for ME/CFS, released in 2015; and
Proposed approach to caring for people who have been diagnosed with ME/CFS.
ME/CFS is a complex, chronic, debilitating illness with systemic effects. It’s characterized by reduced ability to perform activities that were well tolerated pre-illness, accompanied by profound fatigue not improved by rest, and lasting for more than 6 months.
A hallmark of ME/CFS is that symptoms can worsen after physical, mental, or emotional effort, a manifestation known as postexertional malaise. Patients with ME/CFS also have unrefreshing sleep.
Other common symptoms are orthostatic intolerance, cognitive impairment, and pain. As can be observed in people with other long-term chronic illnesses, secondary psychological symptoms such as depression and anxiety may also be present in some patients with ME/CFS.
ME/CFS is a biological illness, not a psychological disorder. Patients with ME/CFS are neither malingering nor seeking secondary gain. These patients have a variety of abnormalities that affect multiple systems, such as:
- Immune and neuroendocrine;
Cellular metabolism; and
Autonomic system regulating blood pressure and heart rate.
A healthcare provider can make the diagnosis of ME/CFS based on a thorough medical history and physical examination, as well as a targeted workup with screening laboratory tests for other fatiguing illnesses.
While there are currently no diagnostic or confirmatory tests, or US Food and Drug Administration–approved drugs specifically for the treatment of ME/CFS, patients benefit from a thorough medical evaluation and good clinical care. Helping patients achieve relief from symptoms and improved quality of life are the main goals of treatment.
In working toward these goals, it’s important to prevent harm that can occur from triggering postexertional malaise. It’s also vital to acknowledge the clinical significance of the condition and to validate the experience and concerns of patients and their loved ones. This acknowledgement often brings patients and families a sense of support and strengthens trust between patients and providers.
It is important to emphasize that anyone can develop ME/CFS. While it is more common in women, and most common in people between 40 and 60 years of age, the illness affects children, adolescents, and adults of both sexes and all ages.
Besides information for healthcare providers, the updated ME/CFS website lists resources for families, patients, and schools, including patients’ personal accounts of living with ME/CFS, called Voice of the Patient.
We invite you to review the information on the website and hope that it will help ensure that clinicians like yourself are informed about how to recognize and manage this debilitating illness. You can provide timely diagnosis and appropriate care for patients with ME/CFS. Thank you.
- CDC: ME/CFS
ME/CFS in Children
ME/CFS Voice of the Patient
CDC: ME/CFS Programs
2015 Institute of Medicine Report on ME/CFS
Public Information from the CDC and Medscape.
Royal College Of Surgeons Blog
Are surgeons missing the major differential diagnosis that is more common than multiple sclerosis and HIV combined?
21 Feb 2019
It’s a great feeling when we meet a new outpatient that we know how to manage surgically. Unfortunately, every surgical specialty experiences a subgroup of patients who present with symptoms that cannot be resolved by surgery. These symptoms may span immune, neurological and vascular systems within the body or brain and may manifest themselves in various ways in several organs at the same time. (See list of symptoms below)
Often these patients have been back-and-forth to the GP or passed on by other medical and surgical specialties. They tend to be the cases that are difficult to diagnose, quantify, understand and detect with routine investigations.
In September 2016, I became ill with acute Epstein Barr Virus Glandular Fever. I continued working, exercising and trying to lead a normal family and social life. I developed all the symptoms listed below, as well as post-exertional malaise (PEM). Every time I tried to do anything challenging (mentally, physically or emotionally) I would experience severe symptom exacerbation and flu-like sore throats with head and neck pain. I couldn’t work, read or watch TV. I couldn’t look after myself, let alone my children, and could barely walk and digest food. Eventually I was diagnosed with Myalgic Encephalomyelitis or Chronic Fatigue Syndrome (ME/CFS).
Myalgic Encephalomyelitis / Chronic Fatigue Syndrome
Often triggered by a viral infection, ME/CFS, can be distinguished from medical and psychiatric conditions by the presence of debilitating fatigue for more than six months and/or combinations of cognitive dysfunction, total body pain, unrefreshing sleep that does not restore normal function and PEM.1
I was never taught about ME/CFS at medical school and it certainly wasn’t in the MRCS examinations that I passed a decade ago. I had a vague notion that it was an illness related to deconditioning, but I was wrong. ME/CFS is a serious neurological condition which can be fatal.
Given that my own prior understanding of ME/CFS was so misguided, I was not surprised to read in the BMJ that 90% of cases of ME/CFS are thought to go undiagnosed, suggesting that people with ME/CFS are substantially undercounted, underdiagnosed and undertreated.2 In another study, 41.9% of ME/CFS patients were told by emergency department staff that it was all in their heads.3 Biobank data suggests ME/CFS is a heritable condition estimated to affect over 286,000 people in the UK; this is more common than multiple sclerosis and HIV combined, and many patients are waiting years for a diagnosis.
On the 24th January 2019, ME/CFS was debated for the first time in 20 years in the main chamber of the House of Commons. It was unanimously agreed that: the Government should provide increased funding for biomedical research into the diagnosis and treatment of ME; the suspension of Graded Exercise Therapy and Cognitive Behavioural Therapy as means of treatment should be supported; GP’s and medical professional’s training needed updating to ensure they are equipped with clear guidance on diagnosis of ME, as well as appropriate management advice to reflect international consensus on best practice and; the current trends of subjecting ME families to unjustified child protection procedures is concerning.4
When you next see a patient with any of the symptoms listed below, ask them about PEM and consider ME/CFS as a differential diagnosis. While they may not leave your clinic with an operation booked, they may finally get a diagnosis, and the time spent in your clinic will have made a big difference to their lives.
Typical symptoms of ME/CFS
· Post Exertional Malaise (PEM)
· Irritable bowel
· Non-specific abdominal pain
· Urinary frequency or urgency
· Facial pain
· Sore throat
· Unrefreshing sleep
· Postural tachycardia and/or orthostatic hypotension
· Nerve pain and tingling
· Bone, muscle and joint pain
· Generalised weakness
· Poor circulation
· Atypical chest pain
· Sensitivity to light, temperature, sound and chemicals
· Difficulty with memory, word finding and multitasking
a) ME Association Index of ME/CFS Published Research
b) Red blood cell deformability is diminished in patients with ME/CFS
c) Widespread brain metabolite abnormalities in ME/CFS
d) Altered gene transcripts
Myalgic Encephalomyelitis: A Baffling Syndrome With A Tragic Aftermath
[This article by Dr Melvin Ramsay (1901 – 1990) was first published in 1986. I thought that it would be helpful, with all the current confusion about ME and mixing it up with various fatigue syndromes and states, to reproduce it here.]
Myalgic Encephalomyelitis: A Baffling Syndrome With A Tragic Aftermath
Melvin Ramsay, M.A., M.D. Hon Consultant Physician,
Infectious diseases Department, Royal Free Hospital
Myalgic Encephalomyelitis leaves a chronic aftermath of debility in a large number of cases. The degree of physical incapacity varies greatly, but the dominant clinical feature of profound [paralytic muscle] fatigue is directly related to the length of time the patient persists in physical effort after its onset; put in another way, those patients who are given a period of enforced rest from the onset have the best prognosis.
Although the onset of the disease may be sudden and without apparent cause, as in those whose first intimation of illness is an alarming attack of acute vertigo, there is practically always a history of recent virus infection associated with upper respiratory tract symptoms though occasionally there is gastro-intestinal upset with nausea and vomiting. Instead of making a normal recovery, the patient is dogged by persistent profound fatigue accompanied by a medley of symptoms such as headache, attacks of giddiness, neck pain, muscle weakness, parasthesiae, frequency of micturition or retention, blurred vision and/or diplopia and a general sense of ‘feeling awful’. Many patients report the occurrence of fainting attacks which abate after a small meal or even a biscuit, and in an outbreak in Finchley, London, in 1964 three patients were admitted to hospital in an unconscious state presumably as a result of acute hypoglycaemia. There is usually a low-grade pyrexia [fever] which quickly subsides. Respiratory symptoms such as sore throat tend to persist or recur at intervals. Routine physical examination and the ordinary run of laboratory investigations usually prove negative and the patient is then often referred for psychiatric opinion. In my experience this seldom proves helpful is often harmful; it is a fact that a few psychiatrists have referred the patient back with a note saying ‘this patient’s problem does not come within my field’. Nevertheless, by this time the unfortunate patient has acquired the label of ‘neurosis’ or ‘personality disorder’ and may be regarded by both doctor and relatives as a chronic nuisance. We have records of three patients in whom the disbelief of their doctors and relatives led to suicide; one of these was a young man of 22 years of age.
The too facile assumption that such an entity – despite a long series of cases extending over several decades – can be attributed to psychological stress is simply untenable. Although the aetiological factor or factors have yet to be established, there are good grounds for postulating that persistent virus infection could be responsible. It is fully accepted that viruses such as herpes simplex and varicella-zoster remain in the tissues from the time of the initial invasion and can be isolated from nerve ganglia post-mortem; to these may be added measles virus, the persistence of which is responsible for subacute sclerosing panencephalitis that may appear several years after the attack and there is a considerable body of circumstantial evidence associating the virus with multiple sclerosis. There should surely be no difficulty in considering the possibility that other viruses may also persist in the tissues. In recent years routine antibody tests on patients suffering from myalgic encephalomyelitis have shown raised titres to Cocksackie B Group viruses. It is fully established that these viruses are the aetiological agents of ‘Epidemic Myalgia’ or ‘Bornholm’s Disease’ and that, together with ECHO viruses, they comprise the commonest known virus invaders of the central nervous system. This must not be taken to imply that Cocksackie viruses are the sole agents of myalgic encephalomyelitis since any generalised virus infection may be followed by a period of post-viral debility. Indeed, the particular invading microbial agent is probably not the most important factor. Recent work suggests that the key to the problem is likely to be found in the abnormal immunological response of the patient to the organism.
A second group of clinical features found in patients suffering from myalgic encephalomyelitis would seem to indicate circulatory disorder. Practically without exception they complain of coldness in the extremities and many are found to have abnormally low temperatures of 94 or 95 degrees F. In a few, these are accompanied by bouts of severe sweating even to the extent of waking during the night lying in a pool of water. A ghostly facial pallor is a well known phenomenon and this has often been detected by relatives some 30 minutes before the patient complains of being ill.
The third component of the diagnostic triad of myalgic encephalomyelitis relates to cerebral activity. Impairment of memory and inability to concentrate are features in every case. Many report difficulty in saying the right word and are conscious of the fact that they continue to say the wrong one, for example ‘cold’ when they mean ‘hot’. Others find that they start a sentence but cannot complete it, while some others have difficulty comprehending the written or spoken word. A complaint of acute hyperacusis is not infrequent; this can be quite intolerable but alternates with periods of normal hearing or actual deafness. Vivid dreams generally in colour are reported by persons with no previous experience of such a phenomenon. Emotional lability is often a feature in a person of previous stable personality, while sudden bouts of uncontrollable weeping may occur. Impairment of judgement and insight in severe cases completes the ‘encephalitic’ component of the syndrome.
I would like to suggest that in all patients suffering from chronic debility for which a satisfactory explanation is not forthcoming a renewed and much closer appraisal of their symptoms should be made. This applies particularly to the dominant clinical feature of profound fatigue. While it is true that there is considerable variation in degree from one day to the next or from one time of the day to another, nevertheless in those patients whose dynamic or conscientious temperaments urge them to continue effort despite profound malaise or in those who, on the false assumption of ‘neurosis’, have been exhorted to ‘snap out of it’ and ‘take plenty of exercise’ the condition finally results in a state of constant exhaustion. This has been amply borne out by a series of painstaking and meticulous studies carried out by a consultant in physical medicine, himself an ME sufferer for 25 years. These show clearly that recovery of muscle power after exertion is unduly prolonged. After moderate exercise, from which a normal person would recover with nothing more than a good night’s rest, an ME patient will require at least 2 to 3 days while after more strenuous exercise the period can be prolonged to 2 or 3 weeks or more. Moreover, if during this recovery phase, there is a further expenditure of energy the effect is cumulative and this is responsible for the unrelieved sense of exhaustion and depression which characterises the chronic case. The greatest degree of muscle weakness is likely to be found in those muscles which are most in use; thus in right- handed persons the muscles of the left hand and arm are found to be stronger than those on the right. Muscle weakness is almost certainly responsible for the delay in accommodation which gives rise to blurred vision and for the characteristic feature of all chronic cases, namely a proneness to drop articles altogether with clumsiness in performing quite simple manoeuvres; the constant dribbling of saliva which is also a feature of chronic cases is due to weakness of the masseter muscles. In some cases, the myalgic element is obvious but in others a careful palpitation of all muscles will often reveal unsuspected minute foci of acute tenderness; these are to be found particularly in the trapezii, gastrocnemii and abdominal rectii muscles.
The clinical picture of myalgic encephalomyelitis has much in common with that of multiple sclerosis but, unlike the latter, the disease is not progressive and the prognosis should therefore be relatively good. However, this is largely dependent on the management of the patient in the early stages of the illness. Those who are given complete rest from the onset do well and this was illustrated by the aforementioned three patients admitted to hospital in an unconscious state; all three recovered completely. Those whose circumstances make adequate rest periods impossible are at a distinct disadvantage, but no effort should be spared to give them the all-essential basis for successful treatment. Since the limitations which the disease imposes vary considerably from case to case, the responsibility for determining these rests upon the patient. Once these are ascertained the patient is advised to fashion a pattern of living that comes well within them. Any excessive physical or mental stress is likely to precipitate a relapse.
It can be said that a long-term research project into the cause of the disease has been launched and there are good grounds for believing that this will demonstrate beyond doubt that the condition is organically determined.
Watch The Debate!
The debate about ME, which was held in the House of Commons, Westminster, London, UK, on Thursday 25 January 2019 can be watched on YouTube; see below. There were a lot of excellent contributions from MPs, many of whom used case histories sent to them by their constituents. Sadly, the one disappointing, weak speech was the response by the Minister of Health. Apart from that, I thought that it was encouraging and well worth watching.
ME Debate In Parliament
From the 25% ME Group website –
Published by Simon Lawrence on 17/01/2019
The Backbench Business Committee has granted a debate on ME. It will take place on the afternoon of Thursday 24th January.
It would be helpful if you could encourage the community to approach their MPs to request their support. Any briefings would also be appreciated.
The motion to be debated next week is as follows: “That this House calls on the Government to provide increased funding for biomedical research into the diagnosis and treatment of ME, supports the suspension of Graded Exercise Therapy and Cognitive Behaviour Therapy as means of treatment, supports updated training of GPs and medical professionals to ensure they are equipped with clear guidance on diagnosis of ME and appropriate management advice to reflect international consensus on best practice, and is concerned about the current trends of subjecting ME families to unjustified child protection procedures.”
Office of Carol Monaghan MP
Member of Parliament for Glasgow North West
Ten Ways To Prove That Exercising Will Not Cure ME/CFS
by Cort Johnson
Your family, friends and even your doctor may, probably will at some point, prod you to get moving. They think that if you can just get on your feet again and start exercising, you’ll be so much better. It’s irritating to hear and just reinforces how isolated you are and how little they understand what you are going through.
You have to cut them some slack, though. You may, after all, look like you’re the picture of health. Plus we all intuitively sense that exercise, in general, is good for us and bedrest can make things worse. From the outside exercise might look like just the ticket. They are only trying to help.
Well, exercise is a ticket – but usually not to better health. While people with ME/CFS – like anybody with a chronic illness – should make every attempt to maintain their fitness, vigorous or even light exercise almost always has negative effects.
But how to convince your family, friends and even your doctor of that? It may take some hard evidence. Below are some suggestions that may help some well-meaning friends, family members and even doctors understand about exercise in chronic fatigue syndrome (ME/CFS).
#1 – Tell them that studies show that your symptoms can get worse – much worse. (They want you to feel better, right?)
Tell them that while vigorous exercise actually reduces pain levels and helps healthy people think better, studies indicate that even bouts of submaximal exercise increase pain sensitivity in ME/CFS and cause more cognitive problems. Vigorous exercise provoked symptoms of fatigue, light-headedness, muscular/joint pain, cognitive dysfunction, headache, nausea, physical weakness, trembling/instability, insomnia, and sore throat/glands in one group of ME/CFS patients.
#2 – Knock out the deconditioning deception, if it shows up.
ME/CFS is not deconditioning nor are its symptoms explained by inactivity. The debility in ME/CFS is much greater than is seen with deconditioning The Workwell Foundation
Yes, but your doctor says those symptoms are occurring because your muscles and cardiovascular system are deconditioned. You just need to get conditioned again!
If only that were so. If you are deconditioned (as is likely if you’re bed or homebound), note that and then tell him/her that a large study just found that deconditioning played no role in the reductions in energy production found during an exercise study. Deconditioning may be present but it’s not causing ME/CFS.
#3 – Point out the negative physiological effects exercising has on ME/CFS.
OK, they say – so exercise makes you feel bad. But shouldn’t you do it anyway? Just to keep up your strength and fitness? Come with me to the gym…
There is certainly something to be said for being as fit as possible in any disease, but studies indicate that vigorous exercise doesn’t just make people with ME/CFS feel worse – it actually damages them physically.
Studies indicate that vigorous exercise impairs an ME/CFS patient’s ability to produce energy and to think, and negatively impacts the functioning of their brain and their autonomic nervous, gastrointestinal, and immune systems. Exercise appears to produce a burst of inflammation in ME/CFS which results in increased oxidative stress and immune, autonomic nervous system and hormonal changes.
In fact, exercise discombobulates so many systems in ME/CFS that it’s regularly used by researchers to understand this illness. A multi-year study underway at the NIH’s Intramural Hospital is using an exercise challenge to do just that.
Thanks, but you’re going to skip the gym…
#4 – Highlight the unique response to exercise found in ME/CFS.
But, but, but, but, but your friend (or doctor) says, people with heart problems, chronic obstructive pulmonary disease (COPD), diabetes, arthritis and other diseases benefit from exercise. People die from heart disease and COPD and they can exercise. Are you saying that ME/CFS is different from all those terrible diseases?
Yes! Tell them that the evidence to date suggests that the exercise problems in chronic fatigue syndrome (ME/CFS) are unique. Unique, as in – not found in any other disease.
Two-day exercise tests indicate that vigorous exercise in ME/CFS actually damages a person’s ability to exercise. That’s very unusual. People with all sorts of serious diseases like heart failure, pulmonary hypertension, and kidney disease can at least tolerate exercise. It’s not so with ME/CFS: the main energy production system in the body (the aerobic energy system) is broken.
#5 – Besides – tell them it’s been tried…and it didn’t work out so well.
Tell them millions of dollars have been spent using an approach called graded exercise therapy (GET) that seeks to have people with ME/CFS exercise more. Tell them that the field is fraught with problems. A recent review of those studies was actually withdrawn by the journal editors because they felt the reviewers overstated their case. Tell them that that rarely happens in the medical field but it’s almost par for the course with regards to GET and ME/CFS.
One huge trial, apparently struggling to get positive results, so dramatically changed their criteria for success that some people with ME/CFS were considered recovered at the time they entered the trial. (Even then the results were mediocre. When another group used the original criteria for success, even those small benefits disappeared.)
Called the PACE trial – the biggest ever in ME/CFS – that study was so poorly done that an entire issue of a medical journal was devoted to exposing its weaknesses. One hundred academics recently signed a letter asking that the results of the trial be re-analyzed.
After a review by an independent group found little evidence that GET works in ME/CFS, the Centers for Disease Control promptly stopped recommending it. This year – the Dutch Health Council – long the bastion of a GET approach to ME/CFS – did the same.
Get the picture? If your doctor thinks they know about exercise and ME/CFS and they’re putting you on a graduated exercise plan that increases your exercise every week, they’re getting some bad information. The GET field is plagued with bad studies which at their best produce mediocre results.
#6 – Maybe you were not a paragon of fitness before ME/CFS showed up… Maybe someone thinks this disease is just the accumulation of insults that you, a couch potato par excellence, somehow foisted upon yourself? If so, tell them about Jamison Hill – bodybuilder extraordinaire.
Jamison Hill was a bodybuilder and athletic trainer before he suddenly, in the midst of a workout, became dizzy, experienced chills and intense heart palpitations – and came down with ME/CFS. Prior to ME/CFS, he spent over 1,500 hours a year working out.
At his worst after ME/CFS, he couldn’t leave his bedroom. Five years later, he’s still homebound with no end to the disease in sight. He’s just one of many former athletes to get it.
#7 – Demonstrate that even gentle exercise can be too much.
OK – your friend says, pounding weights at the gym is out. How about just going for a walk every day. Surely you can do that!
Good try! Some people with ME/CFS can, in fact, go for short walks (and do). Unfortunately, even light exercise like walking is too much for most of us. One study that asked people with ME/CFS to walk 15-25 minutes a day found that instead of getting better, their symptoms worsened. One reason for this is that walking takes more energy than usual in ME/CFS. One study found that walking, presumably because of ME/CFS patients’ reduced ability to utilize oxygen, placed far more of a physiological burden on people with ME/CFS compared to healthy controls.
#7 – Inform them that even normal activities are often too much.
All right, all right, all right – your hubby says. Going on walks isn’t going to do it, but you’re lying in bed most of the time! Surely you can get up and do stuff around the house (????).
If only he knew how much you’d love to do housework. How much you yearn to do the tasks that you didn’t like to do before. You’d LOVE to be able to scrub the floor again!
One study found that the more activity people with ME/CFS engaged in, the more symptomatic they became. Exercise physiologists have found that the aerobic energy production system can be so broken in this disease that even sitting up can be too much.
Even normal activities are often too much. The reason is that ME/CFS is not an exercise disorder, it’s an exertion disorder.
#8 – Emphasize that exercise is just the tip of the iceberg: ME/CFS is really an “exertion” disorder.
Explain that ME/CFS is an exertion disease. In fact, problems with simply exerting oneself, whether physically or mentally, are often so dramatic that a federal report suggested that ME/CFS be called Systemic Exertional Intolerance Disorder (SEID).
New Term – Symptom flares occurring after too much exertion are so bad that a new term – post-exertional malaise (PEM) – was introduced into the medical lexicon to characterize it. PEM is the hallmark symptom of ME/CFS; if normal physical or mental exertion does not cause your symptoms to increase – you don’t have ME/CFS: it’s as simple as that.
Tell him/her studies indicate that too much exertion produces symptoms like exhaustion, brain fog, sleep disturbances, headaches, muscle pain, flu-like symptoms (e.g. nausea, irritable bowel), dizziness, anxiety, depression, and sensory overload. In the worse off, too much exertion can produce a symptom flare that lasts weeks or even months.
#9 – Besides, tell them (politely) that you’d really rather listen to the voices of experience …
Weeks or months? How about years? If they’re still bugging you and you’re not home or bedbound now, you might tell them that about 25% of people with ME/CFS are… and they got that way somehow. The number one response to an informal survey asking people with ME/CFS what they would have done differently, was that they would have paced themselves earlier in the illness. Several thought their lack of pacing set them up for a devastating decline.
#10 – Tell them what can work and how you would love to get some support with that.
At this point your friend may be flustered by all this bad news. Tell them there is one thing that appears to help about 75% of people with ME/CFS. It’s called pacing.
One study found that staying within one’s energy envelope or pacing – staying at a level of activity which does not cause symptoms – allowed many people with ME/CFS to do a bit more with fewer symptoms. Short-term attempts at “pushing through” resulted in crashes (pain and suffering) and less activity overall, while pacing and remaining within one’s energy envelope allowed people with ME/CFS to do more with less pain and fatigue.
Pacing is not a cure, but it can help, and there is an approach to exercise that does work. A heart-rate based exercise protocol which includes pacing and avoids the anaerobic energy production system can help you keep as fit as possible without sending your system into a flare.
Physical therapy – done correctly – can help too. Some patients find that exercises like yoga and QiGong, which keep one limber and emphasize breathing and calming techniques, are beneficial.
From the 25% ME Group: A Patient’s Perspective – Information Leaflet for Professionals Caring for People with Severe M.E. (Myalgic Encephalomyelitis)
SOME FACTS ABOUT SEVERE M.E.
It is important for professionals and carers to remember that this illness can be made worse with physical activity, talking, trying to concentrate or indeed any kind of stimulation or exertion.
Unfortunately this is not widely understood and the misconceptions surrounding this illness can cause additional physical and emotional suffering for those with M.E.
Researchers have demonstrated numerous abnormalities of the immune, muscular, cardiovascular, and central nervous systems. The emerging picture is of a multi-system disease with a strong component of immune and neurological dysfunction. The World Health Organisation recognises M.E. as a neurological illness.
Myalgic Encephalomyelitis (M.E.) describes an illness characterised by a combination of muscle pain (myalgia), and neurological and cognitive symptoms such as memory loss and concentration difficulties (hence ‘encephalomyelitis’).
As with any illness, the symptoms and disability which results will be experienced differently by each individual. Symptoms can vary in severity and commonly include chronic pain and lack of stamina / weakness of the muscles and limbs, acute hypersensitivity to stimuli such as light and noise, cognitive and memory problems, vocal/muscular limitations, multi-joint pain, and severe migraine type headaches.
These are real physical symptoms, which also cause severe distress to the person suffering from them.
The vast majority of severely affected sufferers are virtually housebound or bedbound due to the effects of the disease.
This means their physical and mental limitations are very acute. Commonly the person will require to use a wheelchair to get around, help with transferring from seat to seat within and out with the home, and may have problems with sitting up, using their arms and hands for even simple tasks like doing up buttons on clothing, and have difficulties toileting and bathing themselves. Some very severely affected patients are unable to do any of these tasks because of very severe pain and muscle weakness (not due to misuse or under use) and even transient paralysis – normally down left side. This can leave the person unable even to swallow, or to turn themselves in bed.
SO HOW CAN YOU HELP SEVERE M.E. SUFFERERS?
• People with severe M.E. are asking for no more than other ill people. They need professionals to be aware of the devastating disabling effects of the illness, and its varied symptoms.
• Even severe debility may not be instantly apparent – for example a sufferer may be able to walk to the toilet when required, but unable to sit up in bed for more than a few minutes, watch TV or go out even in a wheelchair, and they may find that they expend most of their energy on something as simple as eating.
• M.E sufferers are happy to arrange for information to be given to any health care or social services professional, if this will help alleviate the current trend of being met with scepticism and disbelief.
• Sufferers need people to respect their experience and knowledge of their own illness. They want to get better – to regain what they have lost. Sadly, complete recovery is rare. Meanwhile the patients are the only ones who know where their limitations lie, and how much they can do without exacerbation.
• Conspicuous deterioration of symptoms after exertion or stimulus –often apparently trivial– is a key feature of this illness. In particular there is a body of research demonstrating abnormal response to exercise and many members of the 25% ME Group have only become severely affected after attempting this. It is important to be aware of the danger of steering patients towards an approach that is highly likely to cause more harm than good.
Please be a responsible professional and carer – to do this you need to listen to what is being said to you by the M.E. patient.
A FINAL MESSAGE
Most importantly, please listen to the person with M.E. There can be harmful consequences for M.E. patients when they are encouraged to push on through the symptoms.
Thank you for your time, please feel free to contact us at the 25% M.E. Group for more information or to use our service as a resource.
If you have any questions, opinions or general concerns that you wish to be addressed, we are more than happy to hear from you. Should you wish to make any comments or submit your views please do so using the form below and return to the address provided on the front of this leaflet. Or you can contact us by e-mail at: email@example.com
The truths of living with severe M.E.
Here Jessica Taylor-Bearman, who has M.E. and is the author of A Girl Behind Dark Glasses, describes her time in hospital from the age of 15 – and how she became determined to document her experience, despite being severe bouts of exhaustion…
When one gets admitted into hospital, it is always thought that it will only be for a short time, whilst they fix you and then you’re back into the whirlwind of real life, so when I was first taken in with very severe M.E., I thought that it would be the same. It wasn’t. Days turned into weeks, that soon became months and years. Four to be exact. I never imagined that I would be hospitalised for such a long time from the age of 15 but there really was no other choice. Despite it being detrimental to my health to be in hospital, my needs could not be catered for in the community.
Hospitals are anything but ideal when you are sensitive to noise to such an extent that even a pin drop hurts, and to light so much so that you had to wear dark glasses all the time, they are hell. It was made even more difficult by the fact for over the half of the time I was there, I could not speak, move or eat. Tubes kept me alive, whilst passive movements were keeping my range up. Being voiceless was the most difficult element because people didn’t understand my needs and unfortunately, didn’t want to give me the time of day.
M.E. is like living with a constant broken battery of energy. There are no Duracell batteries for this bunny! Everything you do costs, whether it be just talking to someone or sitting in a chair. It is all about pacing the day, so you can conserve energy at every opportunity. When I wake up, I must wait for my energy supply to see what will be possible with the day.
Sometimes, I will be able to do some of my paintings or go on a short wheelchair trip and other times, I can be in paralysis for over nine hours, unable to speak or move. One room is often my whole world, and I spend 23 hours at least in bed. This is a huge improvement for me and is one of the reasons I have managed to cope. Back in 2006, the very best I could do was five minutes concentrating on something and I spent all day every day in bed.
Coping with severe M.E. is difficult, and it is hard to feel like you are living a life and not just existing. I do this by concentrating on the really small things and finding joy in them. I had always said I was going to write a book, and to have accomplished that is a massive achievement. I paint through laughter, and this also gives me great happiness. It is incredibly frustrating to not be able to do exactly what you want and to never know how you are going to be on a given day. Life has become a case of surviving through the pain and suffering. We are like butterflies, fighting for our day to break through our cocoons and fly again.
The PACE Trial – A Short Explanation by Graham McPhee
The PACE Trial – A Short Explanation by Graham McPhee. Part 3 – Why it matters.
The PACE Trial – A Short Explanation by Graham McPhee. Part 4 – Where do we go from here?
Grandma with severe Chronic Fatigue Syndrome misses daughter’s wedding and grandchildren’s childhoods
The cruel condition affects 250,000 people in the UK
By John Siddle
An 80-year-old from Farnham has had to skip every family gathering, birthday and Christmas over the past 20 years after a shock diagnosis of a devastating ‘living death’ illness.
Nancy Collins a former NHS nurse was struck down with Myalgic Encephalomyelitis (ME) 20 years ago at the age of 60. She was just months into her retirement after a long and happy 40-year career saving lives.
The disease – also known as Chronic Fatigue Syndrome – is a chronic and fluctuating neurological condition that causes symptoms affecting many of the body’s systems. It most commonly attacks the nervous and immune systems.
One in four sufferers are so severely affected that they were effectively housebound or bedbound.
Debilitated and weak, Nancy finds daily tasks so many of us take for granted impossible and was forced to miss her daughter Sarah Jackson’s wedding in 2011.
She has also had to miss the childhoods of all seven of her grandchildren.
For five years, Nancy could not see anyone as she was so ill she couldn’t stand to pick up the phone.
“It was soul destroying,” a distraught Sarah, 46, said.
She continued: “I couldn’t see her due to the effects of her ME symptoms.
“Mum was in a lot of pain at the time. Just the brain strain of conversations with other people or even people speaking aloud in the same room was intolerable for her.
“The stress of anything outside of her routine was too much. The emotional toll of long term illness and her sadness of what she had lost and was missing out on. She just couldn’t cope.”
Sarah said her mum had had a series of operations and antibiotics prior to being diagnosed.
“Within a year of retiring she started having ME symptoms and it progressively got worse and worse and worse, and she’s now been housebound for about five years,” she explained.
“She’s 80, so it’s difficult to tell what health problems she’d have had anyway.
“She has seven grandkids and only one had been born when she retired, so she has missed out on them all growing up. The youngest is nine.
“She missed my wedding, the birth of my children, every Christmas. We cannot do anything as a family anymore because she cannot have noise, light, she cannot read or do any activities at all. She cannot do anything.
“It’s all just completely overwhelming for her to do anything.”
She added: “Not being able to see her or speak to her for a long period of time was quite soul-destroying and was really difficult. I almost couldn’t talk about it at all because it was too upsetting.”
Sarah now visits her mum every couple of weeks to wash her hair – a task Nancy is too weak to manage alone.
Although she has recently started to sit in the garden and soak up some sunshine, she hasn’t left the house for at least five years and is so weak, she cannot lift a bottle of milk.
Nancy was forced to stay at home when Sarah and Geoff, 44, tied the knot and watched the ceremony via a live link.
However, the sound broke, so she missed hearing their daughter declaring her vows to the love of her life.
Sarah said: “She used to say ‘when you have your children I will be there’ and it just couldn’t happen and she couldn’t be at my wedding.
“She wanted to be there, but just couldn’t.”
Nancy’s heartbreaking daily struggle is made marginally easier by a technique known as pacing.
Sarah explains: “She has a routine and sticks to it, minute by minute. There’s no moving away from the routine, it’s a horrible existence for her and my father.”
Every day, Nancy gets out of bed and dresses because “she thinks it’s important”.
“Everything is very slow and methodical,” said Sarah.
Sarah is sharing the story of how ME has ripped their family apart to raise awareness of the cruel condition so little is known about.
“The problem I think is that it’s not very well researched, it’s difficult to get a diagnosis and there’s a lot of scepticism around the condition – people think it’s psychological.
“It’s debilitating and those people [sufferers] are hidden, they are invisible to society.
“They lay around exhausted, and they may look alright but they’re not alright.”
Sarah said she believes funding difficulties and misinformation online – usually from people claiming they’ve been cured of ME – mean it’s hard for even medical professionals to fully understand what sufferers are going through and how to help them.
“The symptoms are collective and it is a constant battle,” she added.
Honorary medical advisor Charles Shepherd said: “Nancy’s story illustrates just how devastating ME can be and the effect this then has on all aspects of normal family life.
“At best, it leaves people struggling to work or go to school. At worst, it leaves them enduring a tortuous existence, a living death, where they are unable to take their place in society.
“Sadly, many doctors are still uncertain about how to make a diagnosis of ME and how to manage their illness, especially for those like Nancy who have severe ME and are housebound, or even bedbound.
“So those at the severe end of the spectrum and up being severely neglected by both health and social services.”
For more information, visit meassociation.org.uk
A Review of BMJ Best Practice Document on Chronic Fatigue Syndrome by Professor James Baraniuk
[Professor Hooper’s peer-review comments were written to indicate the accurate situation that now obtains concerning the PACE trial raw data. People can judge for themselves if his comments were accepted by the BMJ by looking at their updated version of “Best Practice on CFS” released in September 2018.]
A Review of BMJ Best Practice Document on Chronic Fatigue Syndrome by Professor James Baraniuk
Professor Malcolm Hooper 24th June 2018
NOTE: I was asked by the BMJ Section Editor (BMJ Best Practice and BMJ Learning) to provide a peer review of Professor James Baraniuk’s document on “CFS”, to which I agreed. My comments below relate to the version sent to me. In my opinion, it indicated how dangerous the medical education programme about ME/CFS is in the UK. This was borne out by my face-to-face discussion with Professor Baraniuk himself on 1st June 2018 in London: he confirmed to me that his original report had already been sent by the BMJ to other referees and that he had received 156 comments which he was instructed had to be incorporated in his report. It was plainly obvious that those comments had been included in the version sent to me. Professor Baraniuk assured me that I should go ahead and respond as I wished, so it seems he knew his report was not as he intended it to be. In telephone discussions with the BMJ Section Editor, it was stressed to me that the BMJ had to have (quote) “equality”.
Current BMJ Best Practice for CFS/ME (October 2018):
My response to reading this long document of 102 pages is such that I am unable to carry out the review by simple annotations or minor additions to it.
I am grateful for the invitation to respond by means of a single document that sets out my major concerns which I hope the editor(s) will find helpful.
The document is far too long if it is intended to be a BMJ Best Practice reference tool help GPs and others to quickly diagnose and support their patients presenting with ME/CFS.
As it stands, it is not fit for purpose. The document is badly presented: it needs to be clear and factually accurate.
It lacks focus and any critical awareness of the issues under consideration.
It shows little understanding of the latest research, or the social and political considerations (eg. access to social security payments) that patients and informed clinicians feel so strongly about.
The confusion and complexity of the Best Practice document is far from satisfactory and in need of a thorough overhaul.
It is a wasted opportunity to clarify a situation that has evaded medical education for the last three decades.
2. The Title
The report is entitled “Chronic Fatigue Syndrome” but throughout the text the term “CFS/ME” is used, yet the name myalgic encephalomyelitis does not even feature in the title.
Myalgic Encephalomyelitis (ME) has been classified as a neurological disorder by the World Health Organisation (WHO) in its International Classification of Diseases (ICD) since 1969, but there is no mention of this anywhere in the document.
Throughout the document there is confusion about terminology (ME, CFS/ME, fatigue) but it is essential to be aware that the terms are not clinically interchangeable.
On pages 11, 19, 22, 23, 28, 30, 51 and 102, Baraniuk refers to “CSF/ME”, which appear to be typographical errors, since cerebrospinal fluid (CSF) is not being discussed.
3. Historical perspective
The term myalgic encephalomyelitis was coined in 1955 (Lancet 1955:394-395) and in 1969 it was formally classified by the WHO as a neurological disorder; it was accepted by The Royal Society of Medicine as a distinct disease in 1978; in 1987 the term “chronic fatigue syndrome” was introduced at a meeting of CDC scientists for political, not medical reasons, at which it was decided to change the name from ME to CFS and “CFS” appeared in publications from 1988 onwards.
In 1992 the term “CFS” was included in ICD-10 as a synonym for ME (referable only to ME at G93.3), but in the UK, a group of psychiatrists intended to eradicate the neurological disease ME and introduced the term “CFS/ME” (in that order, as distinct from “ME/CFS”) with their stated intention of dropping “ME” from “CFS/ME” when expedient and then reclassifying “CFS” as a behavioural disorder (BMJ 2003:326:595-597).
In the UK, recruitment for the PACE Trial began in 2004 and the Patient Clinic Leaflet stated: “Chronic fatigue syndrome” is “also known as postviral fatigue syndrome, myalgic encephalomyelitis (ME) or myalgic encephalomyelopathy….Medical authorities are not certain that CFS is exactly the same illness as ME but until scientific evidence shows that they are different they have decided to treat CFS and ME as if they are one illness”.
To complicate things even further, despite his having received ethical approval and funding to include ME in the clinical trial, following publication in 2011 of selective PACE Trial results in The Lancet, the Chief Principal investigator, psychiatrist Professor Peter White, wrote to Richard Horton, editor-in chief of The Lancet, denying outright that the PACE Trial had been studying patients with ME: “The PACE trial paper refers to chronic fatigue syndrome (CFS) which is operationally defined; it does not purport to be studying CFS/ME”.
CFS came to be applied to many different things and considerably broaden the meaning of CFS/ME making it virtually meaningless. Hence, it allowed consideration of other chronic infections, EBV and other herpes viruses, lyme, chlamydia, rickettsia, some vaccines, eg Hep B and latterly HPV and other intracellular organisms eg brucellosis, chemical and environmental toxins, organophosphates, Gulf War Syndrome, Aerotoxic Syndrome, some metals etc. This is ‘confusion worse confounded.’
Clinically, ME is a separate disorder from what is now termed CFS or “CFS/ME”: ME is a recognisable post-enteroviral disease with specific features; it may also follow vaccinations (for which significant evidence already exists and more evidence is emerging). However, there are a number of states of chronic fatigue which now fall under the “CFS/ME” umbrella and the resultant confusion is responsible for the heterogeneity of the patient population and hence the diverse research findings.
Unless the report author provides the contextual background, he affords a disservice not only to the physicians he is endeavouring to educate but – more importantly — to those patients who depend on those clinicians.
4. The way forwards
The term “CFS/ME” now has come to mean a behavioural disorder and this report repeatedly portrays CFS as deconditioning which can be effectively treated by cognitive behavioural therapy (CBT) and graded exercise therapy (GET), but there is no evidence whatsoever of deconditioning in patients with ME/CFS. If this whole document is not based on ME/CFS as a neurological/neuroimmune disorder, then it is falsely grounded.
The report does mention biomedical research, but it appears to look on it sceptically, and the take-home message is clear: “Patients should be educated on how secondary physical deconditioning can emerge due to increased resting and activity restriction” (page 76). This is misleading and it perpetuates the widely-disproven psychosocial dogma that “CFS/ME” is a mental disorder.
It is essential to gain the immediate attention of the reader seeking up-to-date information, so it would be better to start off with a high impact paragraph such as:
“Studies suggest that there is a risk of earlier mortality in ME/CFS and UK Coroners have recorded ME as the cause of death. ME is a serious, disabling, chronic neuroinflammatory disorder: as long ago as August 2004 the US CDC added it to its top priority list of emerging infectious diseases. It is not a behavioural disorder; it is not a form of chronic fatigue (which is not the same as chronic fatigue syndrome as listed in ICD-10 at G93.3), nor is it a form of depression and most patients have no psychiatric disorder. There is a state of chronic, low-grade immune activation, with abnormal T-helper/T-suppressor cells and extremely low NK cell numbers/function; brain abnormalities have been proven, as have neuroendocrine abnormalities. ANS dysfunction is integral to the diagnosis, as is disordered gene expression (important in energy metabolism – metabolomics have convincingly demonstrated defects in pathways converting sugars, lipids and amino acids into energy https://www.youtube.com/watch?v=VprqU9knS4Y). There is evidence of biochemical dysregulation in the 2-5A synthetase/RNASE L pathway (ie. an abnormally elevated anti-viral response). Cardiovascular abnormalities are seminal (including altered brain perfusion, reduced cardiac mass and low circulating blood volume), as is an abnormal response to exercise, with muscle weakness (enteroviral sequences being found in muscle), as well as evidence of impaired oxygen delivery to muscles, with recovery rates for oxygen saturation being 60% lower than in normal controls (Kevin K McCully et al. Clinical Science 1999:97:603-608). Since 2000, patients with ME have been advised to consider taking legal action against health professionals when inappropriate exercise is prescribed. (ME Association). Inability to tolerate medication is well-documented as being virtually pathognomonic (Professor Charles Poser, Department of Neurology, Harvard Medical School, Dublin International Meeting on ME/CFS, 18th-20th May 1994, World Federation of Neurology). There is high occurrence of allergies and hypersensitivities. 25% of patients with ME are severely affected and are bed/house-bound. 80% of patients do not get better: published CDC statistics show only 4% in remission (not recovery) at 24 months (US CDC CFS Programme Update, 29th August 2001)”.
Physicians need to be presented right from the beginning of the document with a clear list of key physical symptoms, but as it stands, the document fails to do so and the author focuses on cognitive problems. He does not mention immune, cardiovascular, neuroendocrine or gastro-intestinal symptoms until much later in the document, whereas from the outset there needs to be a prominent box listing the cardinal symptoms; these include:
post-exertional malaise (PEM); exhaustion; muscle pain and weakness; abdominal pain; diarrhoea; balance disturbance/dizziness; shortness of breath; palpitations; joint pain; easy bruising; allergies/hypersensitivities to foods previously tolerated; chemical sensitivities (including to therapeutic drugs); frequency of micturition including nocturia; visual problems; flushing (not the same as hot flushes); emotional lability; lack of restful sleep and cognitive problems. Pain may be intractable but it may sometimes be absent; hair loss may be total or partial.
To read the rest of the document, please go to –
The impact of profound Multiple Chemical Sensitivity in Severe ME
By Greg Crowhurst
A Painfully Nuanced Life: The impact of profound Multiple Chemical Sensitivity in Severe ME.
(Published in the latest edition of “MCS Aware Magazine”)
‘How can I convey to you that I live in a totally different world than you, even if I am in the same room as you, even if you appear to be in the same physical space as me, believe me I am not experiencing anything in the same way as you.’
This is a very short extract, from my new book: ‘Caring for ME’. It is a quote from my wife.
I am sure that everyone who experiences MCS can relate to what she is saying. Suddenly when you develop MCS, a whole invisible world, previously unknown and unimagined, opens up. Smells and chemicals that others tolerate or do not notice, perfumes that they adore, become a nightmare for you.
In the most extreme cases, it cuts people off completely from normality as it was known, on every level, leaving them totally isolated in a world that torments or harms them. Their symptoms are very painful and difficult to manage.
Suddenly you are in danger from letters in the mail, which often come doused in perfume, from shopping in bags covered in perfume, especially if it delivered via a home delivery scheme, from the fresh air even, saturated by laundry conditioners, barbecue smoke, deodorants that give you a severe headache or cause you to be nauseous, develop rashes and severe symptoms such as throat paralysis.
Suddenly your world becomes painfully nuanced by other people’s lives, in ways that you simply could not have imagined and which those who perpetrate the problem cannot imagine either!
MCS makes an impossible life a nightmare. I have had to become very good at asking any tradesman who has to visit, not to wear any aftershave or perfumed product.
If someone pats our irresistibly cute Corgi, who goes around wagging his tail and making eyes at everyone, it’s horrifying if they are wearing perfume. Hours of torment can follow.
We have not been able to find a mask that my wife can tolerate, her skin is so painful and sore to touch that she cannot bear the pressure. One that we did order had to be hung on the line for days, it smelled so much and was still unusable, sadly.
If I dare go anywhere, I need to shower and change very, very quickly.
MCS; it is a disabling lonely experience.
Into this world, the carer is thrown, having to learn what is unseen. Life with a person with MCS demands that you become acutely aware and sensitive, that you develop skills and practices in order to live with or help the other person to deal with all that is required. Not easy, especially when you cannot even smell the scent that your wife is getting so disturbed by, the one that is going to cause a devastating deterioration in her health and much more disturbance to an already painful and difficult life.
My new book is about caring for people with multiple sensitivities to chemicals, noise, light, movement, touch, food and the host of other agonising; all, disabling symptoms, that are found in Severe ME, yet are so often unseen and unknown by the normal world.
Many people do not have a clue how to approach someone safely. I have been caring for my wife full time for the last 25 years, I am still learning.
How to provide the best care then? It is only possible, we have discovered, by taking a moment by moment approach, seeing what is possible in each moment, dealing with issues that come up as and when it is possible – some moments are too incredibly difficult and painful to achieve anything. Even your presence with the person may be too much. In all moments the greatest possible tenderness and awareness, on the part of the carer is required.
This book is witness to a secret, hidden, tormented existence and unimaginable, intractable suffering, that never ends. That is its starting point. The book is part information, part a journey of self-discovery, through questions designed to challenge and hopefully affirm the carer, helping them identify areas they may need to develop further. I have answered many of the questions myself, to encourage and enable.
“Caring For ME” is a little pocketbook of encouragement and affirmation hopefully for difficult days and happier days alike.
By Greg Crowhurst
Strange as it may sound to some, one of the worst places for a person with ME to be is a hospital, not least because it often leads to a deterioration in health and an increase in symptoms. The noise, light, use of chemicals, a higher risk than usual of catching bugs / infections, and a general lack of understanding about ME, can all cause major problems.
If hospital treatment – either as an inpatient or an outpatient – becomes absolutely necessary, The Grace Charity for ME (www.thegracecharityforme.org) has produced a helpful booklet entitled “Information for patients and hospital staff regarding treatment of patients with ME (Myalgic Encephalomyelitis)”. The booklet includes information about ME and hospital environments, chemicals and drugs (including anaesthetics), surgery, exercise and ME, and diet and allergies.
To download the booklet as a pdf file –
To download as a Word document –
Complaint Report offers hope for those living with ME in Ireland
[This is a long article but well worth reading. I’m posting some of it here; to read the rest, click on the link.]
In this post MEAI Advocate Christine Fenton describes her journey with ME and the HSE, elements of which we’ll all recognise. The Result? Recommendations for actions by the HSE.
I was diagnosed with Myalgic Encephalomyelitis (ME) in 1990 and retired from my career in teaching, a Deputy Head of a high school in the UK, in 2000. Two years later I moved to Ireland to renovate a derelict house and enjoy my passion for dogs and horses.
In 2003 I deteriorated and was surprised that my then GP was dismissive of the ME diagnosis and regarded it as a mental health issue.
By 2006 I was losing the use of my arms and legs, I’d suddenly find myself sitting on the ground as my legs gave way, often with a horse above me! My arms couldn’t manage any repeated use of muscles. I collapsed at an out of hours GP surgery and became paralysed for a short period. The attending GP said she’d never seen anything like this and I should go to Dublin to find the cause.
By chance I had an Out-Patient appointment the week after the collapse and was fortunate to meet with a Consultant new to the local hospital. He was willing to listen and regarded my presentation as an ‘interesting challenge’.
My health continued to deteriorate and from 2011-2016 I was spending approx. 3 months annually in acute care.
The difficulties in achieving a home care package to enable me to access the very limited life I was capable of were legion.
Given the limitations of my body, I needed everything available within arms-reach of my resting place. At that time a wooden steamer chair with settee cushions on it was my bed and day chair.
I also needed a consistent temperature as overheating caused me to be unwell very quickly. If my fingers got cold it would trigger severe pain throughout my body, then my legs would give way and I would end up sitting on the floor, sometimes in an unheated room with no ability to return to a warm, comfortable space. I had to resort to pulling ‘something’ from nearby to cover me to increase my core temperature so that I could recover and crawl/push myself, back to safety.
On the days I was too unwell to move, food had to be beside me, small, easy to digest quantities, taken when I had the energy to put food to my mouth, chew, swallow and digest – you’d never believe how hard the action of eating is, something I took for granted when healthy.
At home, as stairs were beyond me and the bathroom was upstairs I had no facilities available to me. Initially I tried a camping cassette toilet, but it was too heavy to empty and needed emptying too frequently. Often it was full on a day I was struggling to use it, never mind empty it. I needed a better solution which met my needs and capability. I decided to use coal buckets as my toilets. When you live in one room and everything, including eating, is done in that room, a steaming commode is just not welcome – we all know the gut problems which accompany ME. There are some indignities I am not willing to contemplate!
The HSE ‘experts on disability’ were nowhere in sight. My request for support at home had been refused without a visit or an assessment being undertaken, no reason was given to explain why I was not worthy of an assessment. Just a refusal letter from an HSE disability manager who made a judgement without any evidence of my needs on which to base it.
So, I was on my own and had no choice but to create a system which allowed my needs to be met, within the resources available to me.
To continue reading the article, click on –
Letter to Professor Watt of MRC
This letter from Professor Fiona Watt of the Medical Research Council in support of the PACE Trial appeared a few days ago in response to the Times article about the growing pressure on The Lancet concerning the trial:
Sir, Further to your report “Call for review of ‘flawed’ ME research”(Aug 21), as funders of the Pace trial we reject the view that the scientific evidence provided by the trial for using cognitive behavioural theory and managed exercise in the treatment of chronic fatigue syndrome (also known as ME) was unsound. The Pace trial was funded following expert peer review, was overseen by an independent steering committee, and its published findings have also been independently peer-reviewed. Other research groups have drawn similar conclusions. Chronic fatigue syndrome/ME remains a priority for the Medical Research Council (MRC), and it is important that researchers are not discouraged from working on the disease because of concerns that they could be subject to the level of hostility that Pace researchers have experienced. Medical research can only flourish when there is mutual respect between all parties.
Professor Fiona Watt Executive chairwoman, Medical Research Council
There have been other responses from patients. Here is mine, which I decided to send directly to Prof Watt.
Maybe she will see it. Maybe she will read it. Maybe she will do as I ask! I’ve sent it anyhow. You don’t win the lottery if you don’t buy a ticket…
Dear Professor Watt,
Like many patients with M.E. I was surprised and disappointed by your letter to The Times wholeheartedly supporting the PACE trial. There are so many misconceptions in the letter that it is clear that you have not investigated this matter yourself but have – apparently- assumed that what the PACE authors tell you about it is correct and what patients tell you is not. I can only assume that this is because they are doctors and we are merely patients.
Yet you say in your letter that ‘medical research can only flourish when there is mutual respect between all parties’. I would certainly not disagree with that. Please then show patients the respect of being open to the possibility that what we (and indeed many distinguished researchers and other informed parties) say about PACE may actually be correct.
I am not asking you to take us at our word, but please look into the matter yourself instead of simply believing what you are told by the PACE authors and their friends. It will not take you long. I have provided a few references at the end of this letter which you will find useful. For the sake of the patients you say you wish to respect, please take the trouble to do this.
Rethinking the Treatment of Chronic Fatigue Syndrome – A Reanalysis and Evaluation of Findings from a Recent Major Trial of Graded Exercise and CBT by Wilshire et al. – Jan 2018 (A comprehensive re-evaluation of PACE following the release of data from the Freedom of Information Act Tribunal.)
Journal of Health Psychology Vol 22 No.9 Aug 2017 – A Special Issue on PACE. “On the basis of this Special Issue, readers can make up their own minds about the merits and demerits of the PACE Trial,” writes Editor David F Marks.
A letter to The Lancet signed by over a hundred scientists, clinicians, academics, MPs and other experts plus over sixty local, national, and international patient organisations, calling for an independent re-analysis of PACE and setting out the reasons why.
The August 2016 PACE Trial Freedom of Information Tribunal Judgement has useful information about so called hostility to PACE researchers, an unfounded allegation which your letter unfortunately perpetuates.
Two notes relating to this issue:
• Allegations were made at the Tribunal by a representative of the PACE proponents that ME patients, described as ‘activists’ were ‘borderline sociopathic and psychopathic’ and posed ‘a serious threat of violence to trial participants and researchers’ but the Commissioner described these as ‘wild speculations’ which did the representative ‘no credit’ (see pages 22 and 36). PACE researcher Prof Chalder accepted that ‘there had been no threats made either to researchers or participants’ The Commissioner stated that the ‘assessment of activist behaviour was grossly exaggerated. The only actual evidence was that an individual at a seminar had heckled Prof Chalder.’ (see page 40)
• Your letter also suggests that researchers might be ‘discouraged from working on the disease because of concerns that they could be subject to the level of hostility that PACE researchers have experienced’. The idea that researchers are being discouraged in this way is another often repeated misconception which seems to be intended to vilify patients. Working for the MRC, you will be fully aware of how little funding M.E. has received over the years. Nevertheless there is research going on worldwide, strongly supported by patients and often funded by them. (Many of these researchers are critical of PACE and have signed the letter to The Lancet requesting its independent reassessment – see above.) Patients do however object – in the form of letters such as this and other peaceful means – to the squandering of funds on poorly conducted research such as PACE, money which is desperately needed for high quality biomedical research into the condition.
Having ME Is Like Being Permanently Encased In A Suit Of Armour
I have, for a long time, struggled to fully get across the impact this illness has on my life
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.
GP system updated to reflect ME 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.
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.
You and ME: An Update on Myalgic Encephalomyelitis for Psychologists by Rose Silvester
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 illness – NZcare4ME) 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.
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.
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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
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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.
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